Drugs online research references
Mol Urol. 2000 Winter;4(4):415-20.
Terazosin for vesicosphincter dyssynergia in spinal cord-injured male patients.
Bennett JK, Foote J, El-Leithy TR, Saleem MD, Green B, Archer CL, Gray M.
Department of Surgery and Division of Urology, Emory School of Medicine and Shepherd Center, Atlanta, Georgia 30322, USA.
PURPOSE: Evaluation of the role of the long-acting alpha-adrenergic blocker, terazosin, in the treatment of vesicosphincter dyssynergia (VSD) in spinal cord-injured male patients. Patients and METHODS: Sixty spinal cord-injured male patients with VSD were recruited prospectively. Their mean age was 37 years (range 15-70 years). Baseline evaluation included a thorough medical history, clinical examination, blood pressure measurement, intravenous urogram, and videourodynamics. The patients received terazosin for a 90-day period. Videourodynamic evaluation after completion of the study included cystometrogram, sphincter electromyography, maximum urethral pressure gradient (MUPG), and measurement of post voiding residual (PVR) urine volume. The findings were compared with the pretreatment values. RESULTS: Of the 60 patients, 35 completed the study. According to response to treatment, two groups were identified: Group A = responders (N = 17; 49%) and Group B = nonresponders (N = 18, 51%). In Group A, there was a significant decrease in the maximum detrusor pressure, from a mean of 105.3 to 73.9 cm H(2)O, and in MUPG, from a mean of 84.7 to 54.1 cm H(2)O. The bladder capacity and PVR did not change significantly in either group. The time since injury was significantly longer in Group A than in Group B. CONCLUSIONS: Terazosin in a dose of 10 mg/day was well tolerated and effective in reducing bladder outlet obstruction in many spinal cord-injured patients, as reflected by a decrease in maximum detrusor pressure and MUPG in 49% of the patients. Patients with a weak or negative response initially may respond later. Terazosin should be considered a first-line treatment of VSD prior to contemplating surgery.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11156710&dopt=Abstract
Prostate. 2001 Jan 1;46(1):45-51.
Combined effect of terazosin and finasteride on apoptosis, cell proliferation, and transforming growth factor-beta expression in benign prostatic hyperplasia.
Glassman DT, Chon JK, Borkowski A, Jacobs SC, Kyprianou N.
Division of Urology, Department of Surgery, University of Maryland School of Medicine, Baltimore, MD 21201, USA.
BACKGROUND: Medical treatment of benign prostatic hyperplasia (BPH) targets relief of symptoms by causing either relaxation of the prostatic smooth muscle with alpha1 adrenergic blockade, or shrinkage of the gland with 5alpha-reductase inhibitors. We recently demonstrated that alpha1-blockers, such as terazosin, induce apoptosis in prostatic cells. In this study, we examined the combined effect of finasteride and terazosin on the rate of apoptosis and cellular proliferation to investigate their potential synergy at the cellular level. METHODS: Prostate specimens were obtained from men who were treated with either finasteride (n = 24), terazosin (n = 42), or combination therapy (n = 10) for varying time periods (1 week to 36 months) for the relief of the symptoms of BPH. The proliferative and apoptotic indices of both stromal and epithelial prostatic cell populations were determined. Antibodies against TGF-beta1 and TbetaRII were used to examine the immunoreactivity of TGF-beta1 and TbetaRII, respectively, in all prostate tissue sections. RESULTS: The apoptotic index in both prostate cell populations was significantly higher following the combination treatment compared to terazosin or finasteride alone. There were no significant changes in the rate of cellular proliferation with any treatment. Furthermore, there was a significant increase in TGF-beta1 expression in the prostates of patients treated with terazosin or combination therapy, while there was no change in TbetaRII expression. CONCLUSIONS: These results support the concept that induction of prostate apoptosis is a potential molecular mechanism underlying the combination effect of alpha1 blockade with 5alpha-reductase inhibitors in the effective treatment of BPH. The upregulation of TGF-beta1 implies a role for this ligand as an effector of apoptosis induction in response to alpha1-blockade or finasteride therapy of BPH patients. Copyright 2001 Wiley-Liss, Inc.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11170131&dopt=Abstract
Naunyn Schmiedebergs Arch Pharmacol. 2001 Jan;363(1):34-9.
A quantitative analysis of antagonism and inverse agonism at wild-type and constitutively active hamster alpha1B-adrenoceptors.
Hein P, Goepel M, Cotecchia S, Michel MC.
Nephrol. Lab. IG 1, Klinikum Essen, Germany.
In order to characterize inverse agonism at alpha1B-adrenoceptors, we have compared the concentration-response relationships of several quinazoline and non-quinazoline alpha1-adrenoceptor antagonists at cloned hamster wild-type (WT) alpha1B-adrenoceptors and a constitutively active mutant (CAM) thereof upon stable expression in Rat-1 fibroblasts. Receptor activation or inhibition thereof was assessed as [3H]inositol phosphate (IP) accumulation. Quinazoline (alfuzosin, doxazosin, prazosin, terazosin) and non-quinazoline alpha1-adrenoceptor antagonists (BE 2254, SB 216,469, tamsulosin) concentration-dependently inhibited phenylephrine-stimulated IP formation at both WT and CAM with Ki values similar to those previously found in radioligand binding studies. At CAM in the absence of phenylephrine, the quinazolines produced concentration-dependent inhibition of basal IP formation; the maximum inhibition was approximately 55%, and the corresponding EC50 values were slightly smaller than the Ki values. In contrast, BE 2254 produced much less inhibition of basal IP formation, SB 216,469 was close to being a neutral antagonist, and tamsulosin even weakly stimulated IP formation. The inhibitory effects of the quinazolines and BE 2254 as well as the stimulatory effect of tamsulosin were equally blocked by SB 216,469 at CAM. At WT in the absence of phenylephrine, tamsulosin did not cause significant stimulation and none of the other compounds caused significant inhibition of basal IP formation. We conclude that alpha1-adrenoceptor antagonsits with a quinazoline structure exhibit greater efficacy as inverse agonists than those without.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=11191834&dopt=Abstract
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