Drugs online research references
Brain Res. 1998 Feb 23;785(1):75-9.
Central pressor effect of parathyroid hormone-related protein in conscious rats.
Nagao S, Seto S, Kitamura S, Akahoshi M, Kiriyama T, Yano K.
Third Department of Internal Medicine, Nagasaki University School of Medicine, 1-7-1 Sakamoto, Nagasaki 852, Japan.
Although the parathyroid hormone-related protein gene is widely expressed in the central nervous system, the role of this protein in blood pressure is unknown. This article examines whether parathyroid hormone-related protein is involved in the central regulation of blood pressure. An intraventricularly injected solution of parathyroid hormone-related protein elicited a dose-dependent increase of mean arterial pressure accompanied by a decrease of heart rate in conscious Sprague-Dawley rats. An anti-parathyroid hormone-related protein monoclonal antibody, given in an intraventricularly injected solution, blocked the pressor effect of parathyroid hormone-related protein. Furthermore, this pressor effect of parathyroid hormone-related protein was also abolished after pretreatment by intravenous administration of either hexamethonium bromide or doxazosin mesylate. These results suggest that central parathyroid hormone-related protein is implicated in the regulation of blood pressure, and that this effect may be mediated through sympathetic activation. Copyright 1998 Elsevier Science B.V.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9526051&dopt=Abstract
Andrologia. 1998 Feb-Mar;30(1):5-10.
Erectile dysfunction following treatments of benign prostatic hyperplasia: a prospective study.
Uygur MC, Gur E, Arik AI, Altug U, Erol D.
Urology Clinic of the Ministry of Health, Ankara Hospital, Turkey.
The effects of open prostatectomy, transurethral resection, transurethral vaporization, doxazosin and finasteride on sexual functions of men were investigated in a total of 305 patients with benign prostatic hyperplasia. The sexual functions of the patients were assessed with a questionnaire before treatment and 3 and 6 months after the treatment. A total of 212 (70%) patients were judged to be potent before the treatment. At 3 months, open prostatectomy and transurethral resection caused erectile dysfunction in 2 of 40 (5%) and 5 of 89 (6%) potent patients, respectively. At 6 months, one of the patients from the former and 2 of the patients from the latter groups who developed erectile dysfunction at 3 months stated improvement. Transurethral vaporization caused loss of erectile functions in 4 of 14 potent patients (29%) at the 3-month follow-up and, one of these patients recovered erectile functions at 6 months. Only one of the 33 patients (3%) using doxazosin stated that he lost his erectile functions both at 3 months and 6 months. At 3 months follow-up, finasteride caused loss of erectile functions in 8 of 36 potent patients (22%). Four of these patients underwent surgery (transurethral resection) after 3 months of finasteride use. At the 6-month follow-up, 4 more patients suffered from loss of erectile functions. We suggest that finasteride and transurethral vaporization have the greatest potential of impairing the sexual functions among the treatment options investigated in this study and that they must be carefully offered to the potent patients.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9567164&dopt=Abstract
Prostate. 1998 May;35(2):102-8.
Testosterone-induced prostatic growth in the rat causes bladder overactivity unrelated to detrusor hypertrophy.
Pandita RK, Persson K, Hedlund P, Andersson KE.
Department of Clinical Pharmacology, Lund University Hospital, Sweden.
BACKGROUND: Testosterone treatment of rats produces prostatic hypertrophy and detrusor overactivity. Whether or not the detrusor overactivity can be related to an increase in the responsiveness of lower urinary tract smooth muscles is not known. METHODS: Male Sprague-Dawley rats were given daily injections of testosterone propionate for 2 weeks. Effects on cystometric parameters and on the responsiveness of isolated detrusor, urethral, and prostate smooth muscle preparations to drugs and electrical field stimulation were investigated. RESULTS: Testosterone treatment increased prostatic weight twofold (controls, 768 mg; testosterone-treated, 1,478 mg), but not bladder weight (103 mg vs. 116 mg). Micturition pressure (77%), bladder capacity (75%), residual volume (56%), and micturition volume (83%) increased significantly in treated animals, and bladder overactivity developed. No effect of intraarterial doxazosin on these changes was observed. The differences in urodynamic parameters between control and testosterone-treated rats could not be correlated with changes in bladder, urethral, or prostate excitatory innervation, as revealed by responses to electrical field stimulation, or by smooth muscle responses to different contractant drugs. CONCLUSIONS: Some of the urodynamic effects seen after testosterone treatment seem to be caused by the mechanical obstruction of the enlarged prostate. Since there were no changes in smooth muscle responsiveness, it is suggested that the bladder overactivity observed can partly be related to testosterone-induced changes of the micturition reflex at the lower urinary tract, spinal, and/or supraspinal levels.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9568673&dopt=Abstract
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