ADRENERGIC RECEPTOR ANTAGONISTS FIELD OF THE INVENTION The present invention relates to alpha la and/or alpha Id adrenergic receptor antagonists. Compounds disclosed herein can function as alpha la and/or alpha Id adrenergic receptor antagonist and can be used for the treatment of a disease or disorder mediated through alpha la and/or alpha Id adrenergic receptor. Compounds disclosed herein can be used for the treatment of benign prostatic hyperplasia and the related symptoms thereof Compounds disclosed herein can be used for the treatment of lower urinary tract symptoms associated with or without benign prostatic hyperplasia. Process for the preparation of the disclosed compounds, as well as, pharmaceutical composition containing the disclosed compounds, and the methods of treating benign prostatic hyperplasia or related symptoms thereof. BACKGROUND OF THE INVENTION Benign prostatic hyperplasia (BPH) is a condition, wH1ch develops in elderly males and refers to the benign overgrowth of the stromal and epithelial elements of the prostate with aging. The symptoms of BPH vary, but the most common ones involve changes or problems with urination, such as hesitant, interrupted, weak stream or urgency and leaking or dribbling or more frequent urination, especially at night. Consequences of BPH can involve hypertrophy of bladder smooth muscle, a decompensated bladder and an increased incidence of urinary tract infection. There are two components of BPH, static and a dynamic component. The static component is due to enlargement of the prostate gland, wH1ch may result in compression of the urethra and obstruction to the flow of the urine from the bladder. The dynamic component is due to increased smooth muscle tone of the bladder neck and prostate itself and is regulated by a -1 adrenergic receptor. Currently, the most effective treatment for BPH is the surgical procedure of transurethral resection of the prostate (TURP), since it removes the obstructing tissue (C. Chappie's Br. Med. Journal 304: 1198-1199, 1992). It is a treatment, wH1ch is directed to the static and dynamic components of the BPH. However tH1s surgical treatment is associated with rates of mortality (1%) and adverse event (incontinence 2-4%) infection 5-10 %, and impotence 5-10%. A noninvasive alternative treatment is therefore H1ghly desirable. There are some drug therapies, wH1ch address the static component of tH1s condition. Administration of finasteride is one such therapy, wH1ch is indicated for the treatment of symptomatic BPH. TH1s drug is a competitive inH1bitor of the enzyme 5 a-reductase that is responsible for the conversion of testosterone to dihydrotestosterone in the prostate gland. Dihydrotestosterone appears to be the major mitogen for prostate growth, and agents, wH1ch inH1bit 5 a-reductase reduce the size of the prostate and improve urine flow through the prostatic urethra. Although finasteride is a potent 5-a reductase inH1bitor and causes a marked decrease in serum and tissue concentrations of dihydrotestosterone, it is moderately effective in the treatment of symptomatic BPH. The effects of finasteride take 6-12 months to become evident and for many men the clinical development is minimal. The dynamic component of BPH has been addressed by the use of adrenergic receptor blocking agents, wH1ch act by decreasing the smooth muscle tone witH1n the prostate gland. A variety of au AR antagonists, for example, terazosin, doxazosin, prazosin, alfiizosin and tamulosin have been investigated for the treatment of symptomatic bladder outlet obstruction due to BPH. However, these drugs are associated with vascular side effects (e.g. postural hypertention, syncope, dizziness, headache etc) due to lack of selectivity of action between prostatic and vascular ai adrenoceptor. There are several lines of evidence to suggest that selectivity for aia adrenoceptor over aib adrenoceptor will result in relative lack of vascular side effects, thus lead to a better tolerability. Mice deficient in an, adrenoreceptors show diminished blood pressure response to phenylephrine injection compared to homozygous controls (Decreased blood pressure response in mice deficient of ajb adrenergic receptor. (Proc Natl Acad Sci USA 1997,94,11589-11594). In-vivo studies in healthy subjects comparison of aia / aid selective antagonists (for example, tamsulosin) or a^ selective antagonists (for example, urapidil) with non selective antagonists (for example,doxazosin, prazosin, or terazosin) under a variety of experimental conditions (e.g. involving the administration of exogenous agonist or release of endogenous agonist by cold stimulation) in several vascular beds including the skin circulation in finger tips, the dorsal hand vein, or with total peripheral resistance have been reported. (Eur J Clin Pharmacol, 1996, 49, 371-375; Naunyn Schmiedeberg's Arch Pharmacol 1996, 354, 557-561; Jpn J Pharmacol 1999, 80, 209-215; Br J Clin Pharmacol 1999, 47, 67-74). These studies have reported that an antagonist with H1gh affinity for aia or