Drugs online research references
BJU Int. 2000 Feb;85(3):249-53.
The effectiveness of terazosin, an alpha1-blocker, on bladder neck obstruction as assessed by urodynamic hydraulic energy.
Yamanishi T, Yasuda K, Sakakibara R, Hattori T, Tojo M.
Departments of Urology and Neurology, Chiba University, School of Medicine, Chiba, and Department of Urology, Dokkyo University Medical School, Koshigaya Hospital, Saitama, Japan.
OBJECTIVE: To investigate the effectiveness of terazosin, an alpha1-adrenoceptor blocking agent, on bladder neck obstruction (BNO), by assessing the urodynamic hydraulic energy profile. Patients, subjects and methods The study included 17 men (mean age 60.1 years, range 24-84), comprising 11 patients with BNO (mean age 66.5 years) and six normal volunteers (mean age 48.1 years). A five-transducer microtip catheter was used to measure the pressure in the bladder and at the bladder neck, and in the membranous and bulbous urethra during voiding. All the subjects then received terazosin, 1 mg/day orally for 2 weeks, and were re-assessed. RESULTS: The bladder neck diameter at maximum flow significantly (P < 0.02) increased in the 11 patients with BNO after treatment with terazosin. The relative hydraulic energy profiles before terazosin treatment showed the greatest hydraulic energy loss between the membranous and the bulbous urethra in the normal subjects, and between the bladder neck and the membranous urethra in the men with BNO. After terazosin treatment, the greatest energy loss was between the membranous and the bulbous urethra in men with BNO, similar to that in the normal controls, i.e. the whole profile of relative hydraulic energy became normal. CONCLUSION: Terazosin was effective in opening the bladder neck and improving the hydraulic energy profile in men with BNO.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10671877&dopt=Abstract
Urology. 1994 Jul;44(1):52-7.
Effect of alpha 1 adrenoceptor antagonists on prostatic pressure and blood pressure in the anesthetized dog.
Kenny BA, Naylor AM, Carter AJ, Read AM, Greengrass PM, Wyllie MG.
Department of Discovery Biology, Pfizer Central Research, Sandwich, Kent, United Kingdom.
OBJECTIVES. In the current study we have profiled a range of compounds at alpha 1 adrenoceptor subtypes in vitro and have assessed their effects in vivo using the anesthetized dog in an attempt to elucidate the predominant alpha 1 adrenoceptor subtype mediating contractile responses of the canine prostate. METHODS. The affinity of compounds for alpha 1 adrenoceptor subtypes was determined by displacement of [3H] prazosin binding from stably transfected rat 1 fibroblasts expressing alpha 1A, alpha 1B, and alpha 1C, adrenoceptor subtypes. The potency of these agents was then assessed in vivo using an anesthetized dog model allowing simultaneous measurement of prostatic pressure and blood pressure following intravenous (i.v.) administration of phenylephrine (1 to 128 micrograms/kg). RESULTS. All compounds examined in this study showed high and similar affinity for alpha 1 adrenoceptor subtypes, with the exception of 5-Methyl-urapidil, which was selective for alpha 1C (pKi = 9.3) over alpha 1B (pKi = 7.2) and alpha 1A (pKi = 8.1). Doxazosin, terazosin, alfuzosin, and tamsulosin were potent antagonists of phenylephrine responses and in vivo derived "pseudo pA2" determinations showed that the drugs did not discriminate between prostatic and vascular receptors. 5-Methyl-urapidil was also a potent antagonist of phenylephrine-induced responses but was selective for prostatic pressure ("pseudo pA2" = 8.7) over blood pressure ("pseudo pA2" = 7.2). CONCLUSIONS. Data in the present study suggest a predominant role of the alpha 1C adrenoceptor subtype in the contractile response of the canine prostate to phenylephrine in vivo. This model therefore provides a suitable means of assessing putative prostate-selective antagonists for the treatment of benign prostatic hyperplasia.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7913781&dopt=Abstract
Dig Dis Sci. 1994 Nov;39(11):2368-75.
Effect of alpha 1-adrenergic blockade on canine ileal water, electrolyte, and glucose absorption.
Barry MK, Gontarek JD, Pickering SP, Yeo CJ.
Department of Surgery, Johns Hopkins Medical Institutions, Baltimore, Maryland.
Meal ingestion stimulates an increase in small intestinal water and electrolyte absorption. Endogenous norepinephrine may at least partially mediate this meal-stimulated proabsorptive response. Luminally administered alpha 1-adrenergic agonists such as norepinephrine and phenylephrine cause significant small bowel absorption, which can be prevented by the selective alpha 1-adrenergic antagonist terazosin. This study tested two hypotheses: (1) a meal stimulates ileal water, electrolyte, and glucose absorption; and (2) meal-stimulated ileal absorption is mediated via alpha 1-adrenergic receptor activation. Absorption studies (N = 27) were performed on dogs with 25-cm ileal Thirty-Vella fistulas (TVF). Perfusion with [14C]PEG was used to calculate absorption of water, electrolytes, and glucose from the TVF. Three groups were randomly studied over 4 hr: (1) terazosin alone, (2) meal alone, and (3) terazosin plus meal. Terazosin (10(-4) M) was administered to the TVF in groups 1 and 3 following the first hour. A 480-kcal mixed canine meal was ingested at the end of the second hour in groups 2 and 3. Ileal water, electrolyte, and glucose absorption increased significantly in response to meal ingestion (P < 0.05). Luminal terazosin did not significantly alter basal or meal-stimulated ileal absorption. In conclusion, meal ingestion stimulates ileal absorption of water, electrolytes, and glucose. Neither basal nor meal-stimulated ileal absorption is altered by alpha 1-adrenergic receptor blockade. These data suggest that nonadrenergic neural pathways or humoral factors are the likely mediators of meal-induced intestinal absorption.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7956605&dopt=Abstract
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