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FPIN's clinical inquiries. Medical treatment of benign prostatic hyperplasia.
Am Fam Physician. 2008 Mar 1; 77(5): 665-6
Rich KT, Safranek S
Efficacy of an alpha1 blocker in expulsive therapy of lower ureteral stones.
J Endourol. 2008 Jan; 22(1): 41-6
Wang CJ, Huang SW, Chang CH
PURPOSE: To evaluate the clinical role of an alpha(1a-1d)-specific blocker in the medical expulsive therapy of symptomatic lower ureteral stones. MATERIALS AND METHODS: This prospective study was carried out from May 2005 to December 2006 and involved 95 patients. All patients, who had symptomatic lower ureteral stones
J Urol. 2008 Apr; 179(4): 1461-9
Low BY, Liong ML, Yuen KH, Chee C, Leong WS, Chong WL, Khan NA, Cheah PY, Liong KK
PURPOSE: We determined the clinical efficacy and safety of terazosin in the treatment of patients with female lower urinary tract symptoms. MATERIALS AND METHODS: A total of 100 females 20 to 70 years old who met the inclusion criteria of total International Prostate Symptom Score 8 or greater, symptom duration 1 or more months, and did not meet any exclusion criteria were entered into the study. Subjects were randomized to receive terazosin or placebo in titrated dose from 1 mg od, 1 mg twice daily to 2 mg twice daily during 14 weeks. Successful treatment outcomes use primary end point of International Prostate Symptom Score quality of life 2 or less and secondary end point of total International Prostate Symptom Score 7 or less. Other outcome measures included International Prostate Symptom Score individual item scores, King's Health Questionnaire quality of life domains, objective assessment parameters of 24-hour frequency volume chart, maximum flow rate and post-void residual urine. RESULTS: Using a primary end point, 32 of 40 (80%) evaluable terazosin subjects responded in contrast to 22 of 40 (55%) evaluable placebo subjects (p
Hypertension. 2008 Apr; 51(4): 884-90
da Silva AA, do Carmo JM, Kanyicska B, Dubinion J, Brandon E, Hall JE
Previous studies suggest that activation of the CNS melanocortin system reduces appetite while increasing sympathetic activity and arterial pressure. The present study tested whether endogenous activity of the CNS melanocortin 3/4 receptors (MC3/4-R) contributes to elevated arterial pressure in the spontaneously hypertensive rat (SHR), a model of hypertension with increased sympathetic activity. A cannula was placed in the lateral ventricle of male SHR and Wistar (WKY) rats for chronic intracerebroventricular (ICV) infusions (0.5 muL/h). Mean arterial pressure (MAP) and heart rate (HR) were recorded 24 hour/d using telemetry. After 5-day control period, rats were infused with MC3/4-R antagonist (SHU-9119, 1 nmol/h-ICV) for 12 days, followed by 5-day posttreatment period. MC3/4-R antagonism increased food intake in SHR by 90% and in WKY by 125%, resulting in marked weight gain, insulin resistance, and hyperleptinemia in SHR and WKY. Despite weight gain, MC3/4-R antagonism reduced HR in SHR and WKY ( approximately 40 bpm), while lowering MAP to a greater extent in SHR (-22+/-4 mm Hg) than WKY (-4+/-3 mm Hg). SHU9119 treatment failed to cause further reductions in MAP during chronic adrenergic blockade with propranolol and terazosin. These results suggest that endogenous activity of the CNS melanocortin system contributes to the maintenance of adrenergic tone and elevated arterial pressure in SHR even though mRNA levels for POMC and MC4R in the mediobasal hypothalamus were not increased compared to WKY. These results also support the hypothesis that weight gain does not raise arterial pressure in the absence of a functional MC3/4-R.
Bull Exp Biol Med. 2007 Jun; 143(6): 749-52
Filyushina EE, Shmerling MD, Lazarev VA, Buzuyeva II, Markel' AL, Yakobson GS
Comparative morphometrical study of the renal glomerular system was carried out in hypertensive NISAG rats treated with hypotensive drugs during the prepubertal period. Blockade of the renin-angiotensin system with enalapril or losartan during the critical period of ontogeny (the 2nd month of life) produced a long-term hypotensive and renoprotective effect. Treatment with alpha-adrenoblocker terazosin during this period of ontogeny produced a less pronounced hypotensive effect, though with renoprotection. Corinfar (Ca2+ channel blocker) was least effective.
Yonsei Med J. 2007 Dec 31; 48(6): 994-1000
Kwak C, Lee JK, Ku JH
PURPOSE: We determined the efficacy and safety of a relatively high dose of terazosin (5mg) in Korean patients with lower urinary tract symptoms (LUTS), with or without concomitant hypertension. MATERIALS AND METHODS: From July to December 2006, 200 men who consecutively presented with LUTS were prospectively studied. Eight weeks after treatment, blood pressure (BP), uroflowmetry, and International Prostate Symptom Score (I-PSS) were assessed. For analysis purposes, patients were stratified according to concomitant hypertension. Of the 200 patients, 173 completed the scheduled eight-week treatment period. RESULTS: At baseline, no differences were evident in the two groups in terms of I-PSS, Qmax, PVR and BP. After eight weeks of treatment-although I-PSS and uroflowmetry parameters were not significantly different in the two groups-systolic and diastolic BP in the non-hypertensive control group were higher than in the hypertensive group (p= 0.001 and p=0.0100, respectively). Changes in I-PSS, uroflowmetry parameters, and BPs measured at week eight post- treatment commencement did not significantly differ between the two groups. Moreover, the addition of 5mg of terazosin to antihypertensives did not cause a significant reduction in either systolic or diastolic BP in either group. CONCLUSION: Adding terazosin to existing antihypertensive regimens did not seem to increase the incidence of adverse events. Our findings suggest that 5mg terazosin is effective and that it has an acceptable safety profile as an add-on therapy for patients with LUTS and concomitant hypertension.
Acute intoxication with terazosin.
Am J Emerg Med. 2008 Jan; 26(1): 117.e5-6
Seak CJ, Lin CC
alpha(1)-Adrenoceptor antagonists prevent paracetamol-induced hepatotoxicity in mice.
Br J Pharmacol. 2008 Feb; 153(4): 820-30
Randle LE, Sathish JG, Kitteringham NR, Macdonald I, Williams DP, Park BK
BACKGROUND AND PURPOSE: Paracetamol, a major cause of acute liver failure (ALF) represents a significant clinical problem. Adrenoceptor stimulation or antagonism can modulate chemical-induced hepatotoxicity. We investigated the role of endogenous catecholamines and alpha(1)-adrenoceptors in the development of paracetamol- induced hepatotoxicity.EXPERIMENTAL APPROACH: Paracetamol (3.5 mmol kg(-1)) was administered to male CD-1 mice, with and without alpha(1)-adrenoceptor antagonists (prazosin, doxazosin, terazosin and tamsulosin; 35.7 micromol kg(-1)). Serum transaminases and hepatic glutathione (GSH) levels were assessed as markers of hepatic damage. Paracetamol bioactivation was assessed by covalent binding, hepatic and urinary conjugate formation and uridine glucuronosyltransferase activity. Plasma catecholamines levels and hepatic congestion were also analysed. KEY RESULTS: Plasma catecholamine levels were significantly elevated 5 h post paracetamol administration. Prazosin prevented hepatotoxicity when administered 1 h before a toxic paracetamol insult and importantly, when administered up to 1 h post paracetamol injection. Prazosin had no effect on paracetamol-induced depletion of hepatic GSH, paracetamol bioactivation or paracetamol-induced transcription of defence genes. Paracetamol toxicity is associated with marked accumulation of erythrocytes within hepatic sinusoids and prazosin completely prevented this accumulation.CONCLUSION AND IMPLICATIONS: Paracetamol-induced hepatocellular damage is associated with increased circulating catecholamines. alpha(1)-Adrenoceptor antagonists conferred complete protection from paracetamol -induced hepatotoxicity. Protection was associated with absence of hepatic erythrocyte accumulation. Increased catecholamine levels may contribute to the pathophysiology of paracetamol-induced hepatotoxicity by compromising hepatic perfusion. Protection against paracetamol toxicity by alpha(1) antagonists in mice has implications for therapeutic management of patients presenting with paracetamol overdose and ALF.
Lichenoid drug eruption to terazosin.
Br J Dermatol. 2008 Feb; 158(2): 426-7
Koh MJ, Seah PP, Tay YK, Mancer K
Effect of peripheral sympathetic nerve dysfunction on salt sensitivity of arterial pressure.
Clin Exp Pharmacol Physiol. 2008 Mar; 35(3): 273-9
Osborn JW, Collister JP, Guzman P
1. Dysregulation of peripheral sympathetic pathways contributes to some forms of salt-dependent hypertension. However, at the present time it is not known whether salt-induced activation of sympathetic nerves or loss of normal sympathoinhibitory responses to salt-induced volume expansion contributes to neurogenic salt-dependent hypertension. The present study was performed to the test the hypothesis that loss of peripheral sympathetic nerve function results in salt-dependent hypertension. 2. The effect of three pharmacological interventions of sympathetic nerve function on the long-term salt-sensitivity of mean arterial pressure (MAP) were measured: (i) blockade of ganglionic transmission with hexamethonium (HEX; n = 5); (ii) destruction of sympathetic nerve terminals with guanethidine (GUAN; n = 7); and (iii) alpha-adrenoceptor blockade with two specific antagonists, namely prazosin (PRAZ; n = 7) and terazosin (TERAZ; n = 8). 3. Mean arterial pressure and heart rate were measured 24 h/day by radiotelemetry in conscious rats during 5 days of normal and 7 days of high (HNa) dietary sodium intake. Despite marked increases in both sodium and water intake during 7 days of the HNa diet, no statistically significant changes in MAP were observed in HEX, GUAN, PRAZ or TERAZ groups. 4. We conclude that loss of peripheral sympathetic neural pathways alone does not cause salt-dependent hypertension in the rat.