COMBINATION THERAPY FOR LOWER URINARY TRACT SYMPTOMS Field of the Invention This invention relates to combination therapy for the treatment of lower urinary tract symptoms (LUTS) associated with or without benign prostatic hyperplasia (BPH). The combination therapy comprises tailored cti adrenoceptor antagonists, which are selective for ctta over aib subtype but non-selective for a\a over aid subtype, in combination with muscarinic receptor antagonists, preferably bladder selective antagonists, and optionally included 5a-reductase inhibitor for relief of LUTS in a mammal, with or without BPH. Background of the Invention Benign prostatic hyperplasia also known as benign prostatic hypertrophy is highly prevalent in men beyond the age of 50 and increases in severity and incidence with increasing age. The incidence is 70% in 70 years and becomes nearly universal with advancing age with 90% incidence at the age of 80 years [Berry et al, J. Urol, 132:474-479, 1984]. Symptomatic BPH is thought to be due to bladder outflow obstruction and is usually suggestive of the lower urinary tract symptoms [Speakman M.J., Eur. Urol, suppl, 40:21. 2001]. BPH is characterized by nodular enlargement of prostatic tissue and is associated with a variety of bothersome symptoms, which have a negative impact on quality of life. Lower urinary tract symptoms (LUTS) in men includes, but is not, restricted to a complex of obstructive (voiding) and irritative (storage or filling).symptoms, which include increased frequency, nocturia, poor urinary stream and hesitancy or delay in starting urinary flow. Chronic consequences of BPH can include hypertrophy of bladder smooth muscle, a decompensated bladder and increased incidence of urinary tract infections. Histologically, BPH is characterized by glandular (epithelial) and stromal (fibromuscular) hyperplasia with the latter being the dominant factor in the pathogenesis of clinically significant BPH [Shapiro etal.y. Urol, 147: 1293-1297, 1992]. Though the exact etiology of origin of these symptoms is not distinctly clear, two components, a static component and a dynamic component, clearly contribute to obstruction. Prostatic enlargement or hyperplasia of prostate gland physically impinges on the free flow of fluids through the male urethra and leads to varying degrees of bladder obstruction. This component has been referred as the static component [Caine M, /. Urol., 136:1-4, 1986]. increased adrenergic innervation to prostate leads to an increased adrenergic tone of the bladder neck or urethra and is referred to as dynamic component. The irritative symptoms have been closely associated with bladder dysfunction, which was believed to be a consequence of bladder outlet obstruction [Anderson K E, Brit. J. Urol, 85 Suppl: 12-18, 2000]. Standard treatments for BPH involve surgical or pharmacological intervention. Surgical intervention involves removal of the prostate via radical prostectomy or removing the prostate adenoma via transurethral resection of the prostate. These invasive surgical procedures have limited utility because of the morbidity associated with operative procedures as well as the persistence and recurrence of obstructive and irritative symptoms. Surgical procedures are, therefore, not recommended for patients exhibiting mild to moderate symptoms. Presently, pharmacological interventions in the treatment of BPH can be distinctly categorized into two main categories: - alpha-1 adrenergic receptor antagonists and 5-alpha reductase inhibitors. 5-alpha reductase inhibitors such as finasteride and dutasteride reduce the size of prostate [Wilde et al, Drugs, 57:557-581, 1999], thereby alleviating the static component of bladder outlet obstruction. The lesser efficacy associated with these inhibitors is mechanism-based, in that 5-alpha reductase inhibitors decrease the size of prostate by reducing the amount of epithelial tissue without affecting the smooth muscle and the dynamic component of bladder outlet obstruction. Other pharmacological therapy involves the administration of subtype non-selective alpha-1 adrenoceptor antagonists. These agents relax prostatic-urethral smooth muscle by blocking the alpha-1 mediated effects on endogenous tone hence affecting the dynamic component of bladder outlet obstruction and relieving obstructive symptoms [Chappie, Brit J. Urol., 1:47-55, 1995, Kawabe andNiijima, Urol. Int., 42:280-284, 1987, Lepor et al, J. Urol, 148:1467-1474, 1992, Reuther and Aagard, Urol. Int., 39:312-313,1984, Serels and Stein, Neurourol. Urodyn., 17:31-36, 1998]. In addition these alpha-1 adrenoceptor antagonists have also been found to relieve the irritative bladder symptoms associated with BPH. Alpha adrenoceptors are members of a larger G protein-coupled adrenergic receptors family, which mediate the actions of endogenous catecholamines norepinephrme and epinephrine resulting in smooth muscle contraction. cDNA's encoding three distinct alpha-1 adrenoceptor subtype (alpha-la, alpha-lb and alpha-Id) and three distinct alpha-2 adrenoceptor subtypes (alpha-2a, alpha-2b and alpha-2c) have been cloned, expressed stably in cells and resultant protein characterized pharmacologically, [Schwinn et al, J. Pharmacol. Exper. Ther., 272:134-142, 1995, Hieble et al Pharmacol. Rev., £7:267-70, 1995]. Human lower urinary tract contains both alpha-1 and alpha-2 adrenoceptors, with the latter predominating the former [Goepel et al, UroL Res., 25:199-206, 1997]. However the prostatic smooth muscle contraction is mediated predominantly, if not exclusively by alpha-1-adrenoceptors [Hieble et al, Eur. Pharmacol., 107:111 -117, 1985, Chappel et al, Br. J. UroL, 63:487-496, 1989]. Alpha-1 adrenoceptors predominate in prostate and bladder trigone, [Price et al J. UroL, 150:546-551. 1993], and have been shown to be functionally important in mediating smooth muscle contraction [Forray et al, Mol. Pharmacol., 45:703-708, 1994, Lepor et al J. Pharmacol. Exper. Ther., 270:722-727, 1994]. In addition to the three cloned alpha-1 adrenoceptor subtypes, which have high affinity for the prazosin a fourth type of ajAR with low affinity for prazosin (an.) has been postulated [Muramatsu et al, Br. J. UroL, 74: 572-578 (1994)]. However, there is evidence to suggest that it may represent functional phenotype of the alpha-lAR [Daniels D.V., Eur. J. Pharmacol., 370:37-43, 1990]. The non- subtype selective alpha-1 adrenoceptor antagonists, such as prazosin, terazosin, doxazosin and alfuzosin are accompanied by side effects such as postural hypotension, dizziness and syncope. These side effects are attributed to the affinity towards non- selective alpha-1 adrenoceptor subtypes in the vasculature [J. Androl., 18: 345-355, 1991]. Therefore, in an attempt to develop alpha-1 adrenoceptor antagonist with minimal cardiovascular effect, the concept of developing UIA subtype selective antagonists with minimal affinity for V.\Q and CCID subtype in BPH was proposed which is extensively covered in method of use by Synaptic and reviewed in United States Patent Nos. 5,403,847; 5,578,611; 5,780,485; 5,990,128; and 6,015,819. Development of several OCIA subtype selective compounds with minimal affinity for aiB and/or (XID adrenoceptor has been reported. The selectivity at subtype but non-selective for aia over au subtype, in combination with a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally included 5a-reductase inhibitor. The combination may be administered simultaneously, separately or sequentially. Detailed Description of the Invention As used herein the term "tailored ai adrenoceptor antagonists" refer to those agents, which are more than about 20, or more than about 10-fold selective for au as compared to subtype and are less than about 20, or less than about 10 fold selective for a]a over aid subtype AR antagonist in receptor binding and in vitro functional assay. The tailored ai AR antagonists can be selected from, for example: 1 - {3 -[4-(2-methoxyphenyl) piperazin-1 -yl] -propyl} -piperidine-2, 6-dione, 2-[3-{4-(2-isopropoxyphenyl)piperazin-l-yl}propyl]-3a,4,7,7a-tetrahydro-lH-isoindole-l,3(2H)-dione, 5-[2-[[2-(2-ethoxyphenoxy)ethyl]amino]propyl]-2-hydroxybenzenesulfonamide, or their pharmaceutically acceptable salts, pharmaceutically acceptable solvates, enantiomers, racemate, polymorphs, N- oxides or metabolites. In one particular embodiment, the tailored a\ AR antagonists can be selected from, for example: l-{3-[4-(2-methoxyphenyl) piperazin-l-yl]-propyl}-piperidine-2, 6-dione hydrochloride salt, 2-[3 - {4-(2-isopropoxyphenyl)piperazin-1 -yl} propyl] -3a,4,7,7a-tetrahydro-1 H-isoindole-l,3(2H)-dione hydrochloride salt and 5-[2-[[2-(2-ethoxyphenoxy)ethyl]amino]propyl]-2-hydroxybenzenesulfonamide hydrochloride salt. As used herein the term "bladder selective antagonists" refer to those agents, which exhibit greater potency in inhibiting the carbachol-induced response on the bladder than the carbachol-evoked salivation when evaluated simultaneously in in vivo model in rabbit or dog. The bladder-selective antagonists can be selected from, for example: (la, So, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2- cyclopentyl-2-phenyl acetamide, or (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3.1.0}hexyl-6-(methyl)-yl]-2-hydroxy-2,2-diphenyl acetate, (la,5a, 6a)-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(methyl)-yl]-2-hydi-oxy-2-cyclohexyl-2- phenyl acetate, (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3. 1.0]-hexyl-6-(methyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetate, (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide, ( 1 a, 5a, 6a)-N-[3-azabicyclo[3 . 1 ,0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-azabicyclo[3 . 1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide, N-[(la, 5a, 6a)-3-azabicyclo[3.1.0]hex-6-ylmethyl]-2-phenyl-2-hydroxy-2-(N-methyl) phenyl acetamide, N-[(la, 5a, 6a)-3-azabicyclo[3 . 1 ,0]-hex-6-ylmethyl]-2-isopropyl-2-hydroxy-2 -phenyl acetamide, la, 5a, 6a)-3-chloro-3-azabicyclo[3.1.0]hex-6ylmethyl]}-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-[(lRor lS)-3,3-difluorocyclopentyl] -2 -hydroxy-2 -phenyl acetamide, ( 1 a, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3 . 1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclohexyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-(l-phenylethyl)-3-azabicyclo[3. 1.0]hexyl-6-(amino)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide, 3-azabicyclo[3.1.0]hex-3-yl]but-2-ynyl-2-cyclopentyl-2-hydroxyphenyl acetate, N-methyl-N-(la, 5a, 6a)-N-[3-(4-methyl-3-pentenyl)-3-azabicylo[3. 1 .0]-hex-6-yl]-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a,6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(3,4-methylenedioxyphenyl)ethyl)-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-6-N-(3-azabicyclo[3. 1 .0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, or their pharmaceutically acceptable salts, pharmaceutically acceptable solvates, enantiomers, diastereomers, polymorphs, N-oxide or metabolites. In another particular embodiment, the bladder-selective antagonists can be selected from, for example: cyclopentyl-2-phenyl acetamide L-(+)-tartrate salt, (la, Set, 6a)-[3-benzyl-3-azabicyclo[3.1.0}hexyl-6-(methyl)-yl]-2-hydroxy-2,2-diphenyl acetate L(+)-tartrate salt, ( la, 5a, 6a)-[3 -benzyl-3 -azabicyclo[3 . 1 ,0]hexyl-6-(methyl)-yl]-2-hydroxy-2-cyclohexyl-2-phenyl acetate L(+)-tartrate salt, ( la, 5a, 6a)- [3 -benzyl-3 -azabicyclo[3 . 1 ,0]-hexyl-6-(methyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetate L(+)-tartrate salt, (2R)-(+)- (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide L(+)-tartrate salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, (2R)- (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, , 5a, 6a)-N-[3-azabicyclo[3. 1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-(3,3-difluorocyclopentyl)-2-phenyl acetamide tartrate salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide, N-[(la, 5a, 6a)-3-azabicyclo[3. 1 .0]hex-6-ylmethyl]-2-phenyl-2-hydroxy-2-(N-methyl) phenyl acetamide tartrate salt, (2R, 2S)-N-[(la, 5a, 6a)-3-azabicyclo[3.1.0]-hex-6-ylmethyl]-2-isopropyl-2-hydroxy-2-phenyl acetamide hydrochloride salt, , 5a, 6a)-3-chloro-3-azabicyclo[3.1.0]hex-6ylmethyl]}-2-cyclopentyl-2-hydroxy-2-phenyl acetamide hydrochloride salt, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-[(lRor 3,3-difluorocyclopentyl]-2-hydroxy-2-phenyl acetamide tartrate salt, , 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-[(lS or 3,3 -difluorocyclopentyl]-2-hydroxy-2 -phenyl acetamide tartrate salt, (2R, 2S)- (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclohexyl-2-phenyl acetamide succinate salt, (2R, 2S)-(lct, 5cc, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclohexyl-2-phenyl acetamide tartrate salt, (2R, 2S)-(la, 5a, 6a)-N-[3-(l-phenylethyl)-3-azabicyclo[3.1.0]hexyl-6-(araino)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide tartrate salt, (2R)-( 1 a, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide tartrate salt, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide tartrate salt, 2R(+),4[(1R, 5S)-3-azabicyclo[3.1.0]hex-3-yl]but-2-ynyl-2-cyclopentyl-2-hydroxyphenyl acetate hydrochloride, N-methyl-N-(la,5a, 6a)-N-[3-(4-methyl-3-pentenyl)-3-azabicylo[3.1.0]-hex-6-yl]-2-cyclopentyl-2-hydroxy-2-phenyl acetamide L(+) tartrate salt, (2R) (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(3,4-methylenedioxyphenyl)ethyl)-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (2R)- (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide succinate salt, (2R)- (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide L(+) tartrate salt, (1 S)-(3R)-1 -azabicyclo [2,2,2]oct-3 -yl-3,4-dihydro-1 -phenyl-2(l H)-isoquinolinecarboxylate, (1 S)-(3R)-1 -azabicyclo[2,2,2]oct-3 -yl-3,4-dihydro-1 -phenyl-2(l I-I)-isoquinolinecarboxylate succinate salt, 2-methyl propanoic acid 2-[(lR)-3-[bis(l-methylethyl)amino]-l-phenylpropyl]-4-(hydroxymethyl)phenyl ester and 2-methyl propanoic acid 2-[(lR)-3-[bis(l-methylethyl)amino]-l-phenylpropyl]-4-(hydroxymethyl)phenyl ester with (2E)-2-butenedioate. As used herein the term "5a-reductase" refers to enzymes which catalyze the conversion of testosterone (T) to dihydrotestosterone (DHT) in androgen-responsive tissues such as prostate, seminal vesicles, epididymis and skin. Two isoforms of 5a-reductase have been described-Type 1 and Type 2 (Ranjan et al., Life Sci., 71:115-126, 2002). Type 1 5a-reductase is the predominant enzyme in extraprostatic tissues such as skin and liver whereas Type 2 enzyme is predominantly expressed in the prostate. The two enzymes differ in their catalytic and biochemical properties such as Km, pH optimum etc., (Andriole and Kirby, Eur. UroL, 44:82-88, 2003). The 5a-reductase inhibitor may be widely chosen from among those already known to the prior art or subsequently discovered and/or hereafter discovered and/or hereafter developed. Compounds that are inhibitors of testosterone 5a-reductase inhibitor have been disclosed in US 5,595,985, US 4,377,584, US 4,760,071, US 5,017,568, US 5,155,107, US 5,565,467, EP 0572165, WO 93/23420, EP 0572166, WO 93/23050, WO ^3/23038, WO 93/23048, WO 93/23041, WO 93/23040, WO 93/23039, WO93/23376, WO 93/23419, and WO 93/23051, and these patents are incorporated by reference herein in their entirety. Compounds may be inhibitor of a type-1 or type-2 testosterone 5a-reductase isoenzymes or both a type-1 and type-2 or a dual type-1 and type-2. These compounds ca:n be selected from finasteride, dutasteride, epristeride and turosteride, for example. Also provided herein are pharmaceutically acceptable salt of compounds disclosed herein. The pharmaceutically acceptable salts can include, for example, altcali metal salts and addition salts of acids or bases. Suitable pharmaceutically acceptable acid addition salts may be prepared from an inorganic acid or from an organic acid. Example of such inorganic acids include, but are not limited to, hydrochloric, hydrobromic, hydroiodic, nitrous (nitrite salt), nitric (nitrate salt), carbonic, sulfuric, phosphoric acid and like. Appropriate organic acids include, but are not limited to, aliphatic, cycloaliphatic, aromatic, heterocyclic, carboxylic and sulfonic classes of organic acids, such as, for example, formic, acetic, prop ionic, succenic, glycolic, gluconic, lactic, malic, tartaric, dihydroxytartaric acid, citric, ascorbic, glucuronic, maleic, fumeric, pyruvic, aspartic, glutamic, benzoic, anthranilic, mesylic, salicylic, p-hydroxybenzoic, phenylacetic, mandelic, embonic (pamoic), methanesulfonic, ethanesulfonic, benzenesulfonic, pantothenic, toluenesulfonic, 2-hydroxyethanesulfonic, sulfanilic, stearic, algenic, beta-hydroxybutyric, cyclohexylaminosulfonic, galactaric and galacturonic acid and the like. Suitable pharmaceutically acceptable base addition salts include, "but are not limited to, metallic salts made from aluminum, calcium, lithium, magnesium, potassium, sodium and zinc or organic salts made from primary, secondary and tertiary amines, cyclic amines, N,N'-dibenzylethylenediamine, chloroprocaine, choline, diethanolamine, ethylenediamme, and procaine and the like. The salt forms can generally differ from the base forms of the compounds described herein in certain physical properties such as solubility in polar solvent. Prodrugs of these agents are also included. In general, such prodru.gs will be functional derivatives of these compounds, which are readily convertible in. vivo into the required compound. Conventional procedure for the selection and preparation of suitable prodrug derivatives are described, for example, in "Design of Prodrugs", ed. H Bundgaard and, Elsevier, 1985. The present invention also includes metabolites, which become active upon introduction into biological systems. Where the compounds according to the invention have at least one chiral center, they may accordingly exist as enantiomers. Where the compounds according to invention possess two or more chiral centers, they may additionally exist as diastereomers. It is to be understood that all such isomers and racemic mixtures therefore are encompassed within the scope of the present invention. Furthermore, some of the crystalline forms for compounds described herein may exist as polymorphs and as such are intended to be included in the present invention. In addition, some of the compounds described herein may form solvates with water (i.e., hydrates) or common organic solvents. Such solvates are also encompassed within the scope of this invention. In accordance with one aspect, there is provided a product or medicament comprising a pharmaceutically acceptable composition containing a therapeutically effective amount of a tailored cci AR antagonist, which is selective for aia over otib subtype but non-selective for aia over aid subtype, a second pharmaceutically acceptable composition containing therapeutically effective amount of a muscarim'c receptor antagonist, for example, a bladder-selective antagonist and optionally included therapeutically effective amount of 5a-reductase inhibitor as a combined preparation for simultaneous, separate or sequential for the treatment of LUTS with or without BPH. LUTS may include, for example, obstructive symptoms such as hesitancy, poor stream, prolong urination, and feelings of incomplete emptying, and irritative symptoms such as frequency, urgency, nocturia and bladder contractions, in a mammal in need thereof. The term "therapeutically effective amount", as used herein means that amount of active compound that elicits the biological or medicinal response in a mammal which includes at least partial alleviation of the symptoms of the disease being treated. In accordance with a second aspect, there is provided single composition containing a therapeutically effective amount of a tailored cti AR antagonist, which is selective for ctia over aib subtype but non-selective for ocia over a^ subtype, a therapeutically effective amount of a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally a therapeutically effective amount of 5a-reductase inhibitor for the treatment of LUTS with or without BPH. LUTS may include, for example, obstructive symptoms, such as hesitancy, poor stream, prolonged urination and feelings of incomplete emptying, and irritative symptoms such as frequency, urgency, nocturia, and unstable bladder contractions. In accordance with a third aspect, there is provided a pharmaceutical composition containing a tailored ai AR antagonist, which is selective for aia over an> subtype but non-selective for ctia over a^ subtype, a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally 5-alpha reductase inhibitor in combination with pharmaceutically acceptable carriers, diluents or excepients. The compositions disclosed herein include both those containing only one component and those containing a tailored a\ AR antagonist, which is selective for ctia over ctib subtype but non-selective for aja over a^ subtype, a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally included 5a-reductase inhibitor and which, may be suitable for oral, parenteral, topical, transdermal, cholonic or intravaginal administration. The composition may be formulated to provide immediate or sustained release of the therapeutic agents. The agents described herein can be administered alone but will generally be administered as an admixture with a suitable "pharmaceutically acceptable carrier". The term "pharmaceutically acceptable carrier" is intended to include non-toxic, inert solid, semi-solid or liquid filter, diluent, encapsulating material or formulation auxiliary of any type. Solid form preparations for oral administration may include capsules, tablets, pills, powders, granules and suppositories. For solid-form preparations, the active compound is mixed with at least one inert, pharmaceutically acceptable excipient or carrier such as sodium citrate, dicalcium phosphate and/or a filter an extender such as starch, lactose, sucrose, glucose, mannitol and silicic acid; binders such as carboxymethyl cellulose, alginates, gelatins, polyvinylpyrrolidinone, sucrose, acacia; disintegrating agents such as agar-agar, calcium carbonate, potato starch, aliginic acid, certain silicates and sodium carbonate; absorption accelators such as quaternary ammonium compounds; wetting agents such as cetyl alcohol, glycerol, monostearate; adsorbents such as kaolin; lubricants such as talc, calcium stearate, magnesium stearate, solid polyethyleneglycol, sodium lauryl sulphate and mixtures thereof. In case of capsules, tablets, or pills, the dosage form may also comprise buffering agents. The solid preparation of tablets, capsules, pills, granules can be prepared with coatings and shells, such as enteric coating and other coatings well known in the pharmaceutical formulating art. Liquid-form preparations for oral administration can include pharmaceutically acceptable emulsions, solution, suspensions, syrups and elixirs. For liquid-form preparatioixs, the active compound can be mixed with water or other solvent, solubilizing agents and emulsifiers such as ethyl alcohol, isopropyl alcohol, ethyl carbonate, ethyl acetate, benzyl alcohol, benzyl benzoate, propylene glycol, 1,3-butylene glycol, dimethylformamide, oils (such as cottonseed, groundnut, corn, germ, olive, castor and sesame oil), glycerol and fatty acid ester of sorbitan and mixtures thereof. Besides inert diluents, oral compositions can also include adjuvants such as wetting agents, emulsifying agents, suspending agents, sweetening agents, flavoring agents and perfuming agents. Injectible preparations such as sterile injections, aqueous or oleaginous suspensions may be formulated according to the art using suitable dispersing or wetting and suspending agents. Among the acceptable vehicles and solvents that may be employed are water, Ringers solution and isotonic sodium chloride. Dosage forms for topical or transdermal administration can include ointments, pastes, creams, lotions, gel, powders, solutions, sprays, inhalants or patches. The active compound can be admixed under sterile conditions with a pharmaceutically acceptable carrier and preservatives or buffers as may be required. The pharmaceutical preparations can be in unit dosage form. In such form, the preparation can be subdivided into unit doses containing appropriate quantities of the active component The formulations as described herein may be formulated so as to provide quick, sustained, or delayed release of the active ingredient after administration to the patient by employing procedures well known to the art. The compositions may be administered as a depot formulation that permits sustained release, limits access to general circulation, and increases the prostate and/or bladder-specific localization of the composition. Such formulations may be provided as slow release implants, be microencapsulated, or attached to biodegradable polymers or prostate-specific immunoglobulins. The compound can be administered in a sustained release formulation as a tablet or capsule. A sustained release formulation is a preparation that releases the active component over a desired period of time after administration. A sustained release formulation is prepared by applying a biodegradable, bioerodible or bioabsorbable polymeric formulation that is compatible on the surface of the active component. Examples of sustained release formulation include, but are not limited to, hydroxypropylmethylcellulose (HPMC), hydrogenated vegetable oil (HVO), ethyl cellulose, polyvinylpyrrolidione, pyran copolymer, polyhydroxypropylmethacryl -amidephenol, polyhydroxy - ethylaspartamidephenol, or polyethyleneoxidepolylysin substituted with palmitoyl residues, polylactic acid, polyepsilon caprolactone, polyhydroxy butyric acid, polyorthoesters, polyacetals, polydihydro-pyrans, and polycyano acrylates. The term "biodegradable" means that the polymeric formulation degrades over time by the action of enzymes, by hydrolytic action and/or by other mechanisms in the human body. By "bioerodible" it is meant that the polymeric formulation erodes or degrades over time due, at least in part, to contact with substances found in the surrounding tissue fluids or cellular action. By "bioabsorbable", it is meant that the polymeric formulation is broken down and absorbed within the body of a mammal, for example, by a cell or tissue. "Biocompatible" means that the polymeric formulation does not cause substantial tissue irritation or necrosis. The compounds described herein can also be administered in the form of liposome delivery systems, for example, small unilamellar vesicles, large unilamellar vesicles and multilamellar vesicles. Liposomes can be formed from a variety of phospholipids, for example, cholesterol, stearylamine or phosphatidylcholines. Herein are also disclosed aqueous parenteral compositions, containing a therapeutically effective amount of a tailored ai AR antagonist, which is selective for ctia over ct|b subtype but non-selective for aia over aid subtype, a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally included 5-alpha reductase inhibitor. The invention also provides a method of delivery such that direct intraprostatic injection of a therapeutically effective amount of disclosed compositions results in the relief of obstructive symptoms associated with benign prostatic hyperplasia. Also disclosed herein is a method of treating LUTS with or without BPH. LUTS may include, for example, obstructive symptoms such as hesitancy, poor stream, prolonged urination, and feelings of incomplete emptying, and irritative symptoms such as frequency, urgency, nocturia and bladder contractions caused by BPH, comprising the administration of a therapeutically effective amount of a tailored oci AR antagonist, which is selective for ctia over ctib subtype but non-selective for ctu over aid subtype, therapeutically effective amount of a muscarinic receptor antagonist, for example, a bladder-selective antagonist and optionally included 5a-reductase inhibitor to mammal in need thereof. The combined preparation can be administered simultaneously, separately or sequentially. As used herein the term "combined preparation" refers to a product or medicament comprises a container (packaging device well known to one ordinary skilled in the art) containing separate pharmaceutical compositions [same or different dosage forms, for example, oral (such as capsules, tablets, pills, powder, granules, suppository, emulsions, solution, suspensions, syrups or elixirs), injectible, topical or transdermal (such as ointments, pastes, creams, lotions, gel, powders, solutions, spray, inhalants or patches) of tailored cti adrenoceptor antagonist, bladder selective antagonist and optionally 5a-reductase inhibitor. Also disclosed herein is a method for the treatment of LUTS with or without BPH, comprising administering a single dosage form containing a therapeutically effective amount of a tailored ai AR antagonist, which is selective for CL\& over aib subtype but non-selective for ecu over aid subtype, therapeutically effective amount of a muscarinic receptor antagonist, for example, a bladder-selective antagonist, and optionally included 5a-reductase inhibitor to a mammal in need thereof. The suitability of a tailored ai AR antagonist in this invention can be determined using for example, the assay methods those disclosed in J. Auton. Pharmacol., 16:21,1996. The suitability of a muscarinic receptor antagonist, for example, a bladder selective antagonist in this invention can be determined using for example the assay methods those disclosed in Life Set., 64:2351, 1999 and J. Med. Chem., 42:1999, 1999. The pharmaceutical compositions as described herein can be administered together combined in a single dosage form or they can be administered separately, simultaneously or sequentially, each in its dosage form but as part of the same therapeutic treatment program or regimen. Separate administration of each compound, at different times and by different routes, will sometimes be recommended. Other pharmaceutical components may also optionally be included as part of the combination for the treatment of BPH and LUTS associated with or without BPH. WE CLAIM: 1. A pharmaceutical composition comprising a tailored ai-adrenoceptor antagonist, a bladder selective antagonist and optionally included 5cc-reductase inhibitor, optionally together with pharmaceutically acceptable carriers, excipients or diluents. 2. The pharmaceutical composition according to claim 1 wherein the tailored cti AR antagonist is selective for ctia over aib subtype but non-selective for aja over aid subtype. 3. The pharmaceutical composition according to claim 1 wherein the tailored cci AR antagonist is more than about 10 fold selective for aia over aib subtype and is less than about 10 fold selective for otia over aid subtype in receptor binding and in vitro functional assay. 4. The pharmaceutical composition according to claim 3 wherein the tailored cti adrenoceptor antagonist is selected from: 1 - {3-[4-(2-methoxyphenyl) piperazin-1 -yl]-propyl} -piperidine-2, 6-dione, 2-[3-{4-(2-isopropoxyphenyl)piperazin-l-yl}propyl]-3a,4,7,7a-tetrahydro-lH-isoindole-l,3(2H)-dione, 5-[2-[[2-(2-ethoxyphenoxy)ethyl]amino]propyl]-2-hydroxybenzenesulfonamide, and their pharmaceutically acceptable salts, pharmaceutically acceptable solvates, enantiomer, racemate, polymorphs, N- oxides or metabolites. 5. The pharmaceutical composition according to claim 3 wherein the tailored oti adrenoceptor antagonist is selected from: l-{3-[4-(2-methoxyphenyl) piperazin-l-yl]-propyl}-piperidine-2, 6-dione hydrochloride salt, 2-[3-{4-(2-isopropoxyphenyl)piperazin-l-yl}propyl]-3a,4,7,7a-tetrahydro-lH-isoindole-1,3(2H)-dione hydrochloride salt and 5-[2-[[2-(2-ethoxyphenoxy)ethyl]amino]propyl]-2-hydroxybenzenesulfonamide hydrochloride salt. 6. The pharmaceutical composition according to claim 1, wherein the bladder selective antagonist is an agent which exhibits greater potency in inhibiting the carbachol-induced response on the bladder than the carbachol-evoked salivation when evaluated simultaneously in in vivo model in rabbit or dog. 7. The pharmaceutical composition according to claim 6 wherein the bladder selective antagonist is selected from: (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3. 1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3.1 .0}hexyl-6-(methyl)-yl]-2-hydroxy-2,2-diphenyl acetate, (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(methyl)-yl]-2-hydroxy-2- cyclohexyl-2-phenyl acetate, (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3.1 .0]-hexyl-6-(methyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetate, (la, 5a, 6a)-N-[3-azabicyclo[3.1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2- cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-azabicyclo[3.1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2- cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide, N-[(la, 5a, 6a)-3-azabicyclo[3.1.0]hex-6-ylmethyl]-2-phenyl-2-hydroxy-2-(N-methyl) phenyl acetamide, N-[(la, 5a, 6a)-3-azabicyclo[3.1.0]-hex-6-ylmethyl]-2-isopropyl-2-hydroxy-2-phenyl acetamide, a, 5a, 6a)-3-chloro-3-azabicyclo[3.1.0]hex-6ylmethyl]}-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-[(lR or 1S)-3,3-difluorocyclopentyl]-2-hydroxy-2-piienyl acetamide, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclohexyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-(l-phenylethyl)-3-azabicyclo[3.1.0]hexyl-6-(amino)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide, (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide, 3-azabicyclo[3.1.0]hex-3-yl]but-2-ynyl-2-cyclopentyl-2-hydroxyphenyl acetate, N-methyl-N-(la, 5a, 6a)-N-[3-(4-methyl-3-pentenyl)-3-azabicylo[3.1.0]-hex-6-yl]-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(3,4-methylenedioxyphenyl)ethyl)-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, (la, 5a, 6a)-6-N-(3-azabicyclo[3.1.0]hexyl-3-(4-methyl-3-pentenyl))-2-cyclopentyl-2-hydroxy-2-phenyl acetamide, and their pharmaceutically acceptable salts, pharmaceutically acceptable solvates, enantiomers, diastereomers, polymorphs, N-oxide or metabolites. 8. The pharmaceutical composition according to claim 6 wherein the bladder selective antagonist is selected from: (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3. 1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide L-(+)-tartrate salt, (la, 5 a, 6a)- [3-benzyl-3 -azabicyclo [3 .1.0} hexyl-6-(methyl)-yl] -2-hydroxy-2,2-diphenyl acetate L(+)-tartrate salt, (la, 5a, 6a)- [3 -benzyl-3 -azabicyclo [3.1 .0]hexyl-6-(methyl)-yl]-2-hydroxy-2- cyclohexyl-2-phenyl acetate L(+)-tartrate salt, (la, 5a, 6a)-[3-benzyl-3-azabicyclo[3.1 .0]-hexyl-6-(methyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetate L(+)-tartrate salt, +)- (la, 5a, 6a)-N-[3-benzyl-3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide L(+)-tartrate salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, (2R)- (la, 5a, 6a)-N- [3 -azabicyclo [3.1.0] hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, (2S)-(la, 5a, 6a)-N- [3 -azabicyclo [3.1 .0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-cyclopentyl-2-phenyl acetamide hydrochloride salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2-(3,3-difluorocyclopentyl)-2-phenyl acetamide tartrate salt, (2R, 2S) (la, 5a, 6a)-N-[3-azabicyclo[3.1.0]hexyl-6-(aminomethyl)-yl]-2-hydroxy-2,2-diphenyl acetamide N-[(la, 5a, 6a)-3-azabicyclo[3. 1 .0]hex-6-ylmethyl]-2-phenyl-2-hydroxy-2-(N-methyl) phenyl acetamide tartrate salt, (2R, 2S)-N-[(la, 5