Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0012833 (dizziness)
 9,689 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The specific competitive alpha 1-postsynaptic blocking action and haemodynamic effects of prazosin (Minipress) have been summarized. Prazosin causes dilatation of arterioles and veins, reduces total peripheral resistance as well as preload and afterload. Cardiac output does not change at rest, stroke volume and subsequent cardiac output increase during exercise. The changes in heart rate have non-significant. It does not cause sympathetic counter-regulation, plasma renin activity does not increase, aldosterone level decreases, salt- and fluid retention may rarely be observed. It does not provoke angina. The authors report on the results of their examinations with the first dose of prazosin in 61 patients (in 33 cases by the double-blind cross-over method by placebo control), and summarize the observations made with the drug in long-term treatment in Hungary. The authors and other teams used prazosin as a long-term treatment (of approximately 3 months) in combination with other drugs in a total of 344 patients, and as monotherapy in 159 patients. In the course of combination treatment side-effects were observed in 15% of the patients (dizziness, headache, weakness, occasionally palpitation). During monotherapy, side-effects occurred in 12% of the patients (tachycardia, headache, weakness, dizziness). Hungarian results confirm the usefulness of prazosin in all stages of hypertension. It is effective in 30-35% of the cases as a monotherapy (this rate is congruent with the efficacy of beta-blockers, calcium antagonists and antihypertensive drugs of central action). Earlier prazosin had been used as a third agent in combination treatment of hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The mechanism of the action of Minipress. Examinations in hypertension. 257 64

The efficacy and safety of prazosin GITS (gastro-intestinal therapeutic system), a new extended-release once-a-day formulation, were assessed both as monotherapy in mild essential hypertension and in combination with a diuretic in moderate essential hypertension in two multicenter, double-blind, placebo-controlled trials. Prazosin GITS (Minipress XL) given once daily in doses of either 10 or 20 mg significantly reduced sitting and standing systolic and diastolic blood pressure compared with placebo in both mild and moderate essential hypertension. There were minimal, clinically insignificant changes in heart rate following prazosin-GITS treatment (2.5, 10, and 20 mg) compared with placebo treatment. Prazosin GITS was well tolerated; the most common adverse experiences reported were headache, dizziness, and fatigue. All adverse experiences in the moderate hypertension group and the majority (91 percent) in the mild hypertension group were mild-to-moderate in severity. The results from these multicenter trials demonstrate the efficacy and safety of this new extended-release once-a-day formulation of prazosin in the treatment of patients with mild and moderate essential hypertension.
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PMID:Efficacy and safety of Minipress XL, a new once-a-day formulation of prazosin. 266 73

Recent reports have shown that beta-adrenergic blockade may exacerbate variant angina. On theoretical grounds, alpha-adrenergic blockade may be beneficial in these patients. To test this hypothesis, we assessed the efficacy of prazosin, an alpha-adrenergic blocking agent, in six men, mean age 49 years, with variant angina. Prazosin, 14.0 +/- 2.4 mg/day (mean +/- SD) in three equal doses, was compared with placebo in a double-blind, randomized, double-crossover trial lasting 4 1/2 months: 2 weeks of open-label prazosin followed by four 1-month periods of blinded alternating therapy. No other vasoactive medications were administered during the study. Prazosin reduced sitting systolic arterial pressure from 145 +/- 18 to 127 +/- 16 mm Hg (p = 0.02), but exerted no effect on diastolic arterial pressure or heart rate. Prazosin did not change the weekly number of episodes of chest pain (2.5 +/- 2.3 with placebo vs 3.1 +/- 3.0 with prazosin, NS), nitroglycerin tablets used (3.9 +/- 3.7 with placebo vs 4.6 +/- 4.2 with prazosin, NS), or transient ST-segment deviations (by calibrated two-channel Holter monitoring for 24 hours/week throughout the study) (6.5 +/- 10.1 with placebo vs 11.8 +/- 17.4 with prazosin, NS). During prazosin therapy, three patients had orthostatic dizziness and one patient had headache. Thus, in a long-term, randomized, double-blind trial, prazosin exerted no obvious beneficial effect in patients with variant angina.
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PMID:Alpha-adrenergic blockade for variant angina: a long-term, double-blind, randomized trial. 613 37

The selective alpha, blocker prazosin was used to abolish Prinzmetal's variant angina in six patients. All had had an acute transmural myocardial infarction, after which the anginal attacks with transient ST segment elevation developed, and three of them had already suffered from variant angina prior to the infarction. Therapeutic trials with high doses of nifedipine, verapamil, nitrates, beta blockers, and (in one case) phenoxybenzamine were ineffective in all six patients. Prazosin, 8 to 30 mg/day combined with low-dose nitrates or nifedipine completely abolished the attacks in four patients, markedly reduced their frequency and intensity in one patient, and had to be stopped in the sixth one because of hypotension and dizziness. Except for this last patient, the drug was well tolerated by all the others, and no changes in blood pressure were observed. In four patients discontinuation or reduction of prazosin resulted in exacerbation of symptoms, but its renewal was followed by disappearance of the attacks. Since the mean follow-up period in this study was 4 to 6 months, further evaluation appears necessary concerning the long-term effects of this drug in Prinzmetal's variant angina.
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PMID:Prazosin therapy for refractory variant angina. 682 8

Twelve patients with severe chronic congestive heart failure (CHF) (NYHA class III and IV) resistant to digitalis and diuretics were treated with the postsynaptic alpha-blocking agent prazosin (PZ) (3 to 20 mg/day). In 11 patients oral PZ treatment was well tolerated; the agent was discontinued in the remaining patient because of orthostatic dizziness. After 4 weeks of PZ, total systemic vascular resistance decreased from 2245 +/- 792 to 1603 +/- 355 dyn sec cm-5, mean blood pressure declined from 100 +/- 15 to 90 +/- 14 mm Hg, and pulmonary capillary wedge pressure decreased from 29 +/- 8 to 25 +/- 9 mm Hg. Cardiac index increased from 1.92 +/- 0.63 to 2.30 +/- 0.41 l/min/m2. The increase of stroke volume index correlated with the fall in peripheral vascular resistance (r = --0.79, p less than 0.01) and the decline in pulmonary capillary wedge pressure (r = --0.75, p less than 0.05). In parallel, exercise tolerance increased significantly. Four patients improved from functional class IV to II, four from class IV to III, and one from class III to II, while two patients were unchanged. In the eight patients followed for 6 months, the beneficial effects of ambulatory PZ were maintained throughout the expansive observation period. Three patients died as their disease process progressed during the study (sudden death, pneumonia, and post-PZ withdrawal pump failure). Prazosin is a valuable vasodilator for long-term treatment of otherwise refractory congestive heart failure with the agent given in sufficient individualized dosage.
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PMID:Sustained effectiveness of chronic prazosin therapy in severe chronic congestive heart failure. 722 92

Earlier nonselective alpha 1-adrenergic blocking drugs such as phentolamine and phenoxybenzamine are now restricted to the pharmacological management of alpha 1-adrenergic crisis and phaeochromocytoma. Prazosin, the first selective alpha 1-blocker approved for the treatment of hypertension, became available in the mid-1970s. Additional alpha 1-blockers such as doxazosin and terazosin have been introduced during recent years. The undesirable effects of all members of this class are similar. Most adverse events can be attributed to reversible competitive antagonism of postsynaptic alpha 1-adrenergic receptors in tissues that sustain high levels of alpha-adrenergic sympathetic tone, e.g. resistance arteries, capacitance veins and the urinary bladder outflow tract. Orthostatic hypotension with a sensation of intense faintness and occasional syncope, can occur shortly after the initial dose. Aggravating factors include upright posture, intravascular volume depletion and concurrent administration of other medications that lower blood pressure, including all other classes of antihypertensive drugs. The problem is reduced or avoided by the choice of low starting doses, beginning treatment at bedtime and by minimising other risks. Among overall adverse effects, asthenia, dizziness, faintness and syncope predominate and occur in 10 to 20% of patients, leading to discontinuation of therapy in about half that number. Infrequent adverse events include headache, drowsiness, palpitations, urinary incontinence and priapism. Some patients experience a 1 to 2kg bodyweight gain which may be associated with secondary hyperaldosteronism. Tolerance appears to develop to the benefits of alpha 1-blockade in patients with congestive heart failure, but not in hypertension.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Adverse effects of alpha 1-adrenergic blocking drugs. 791 78

Effective renal plasma flow (ERPF) and glomerular filtration rate (GFR) were measured in 53 hypertensive patients (26 renally impaired, 27 with normal renal function) before and after treatment with sufficient bunazosin retard or prazosin to control their high blood pressure. After a 3-week placebo run-in period, patients were classified as normal (creatinine clearance > 80 ml/min) or renally impaired (20-55 ml/min), and randomly assigned to bunazosin retard or prazosin. There followed a dose titration (T) phase of 6-7 weeks, and a maintenance (M) phase of 4 weeks. Blood pressure was satisfactorily controlled (sitting diastolic pressure < or = 90 mmHg or decreased by > or = 10 mmHg) by both drugs in both groups. Bunazosin Retard was associated with increases in GFR and ERPF in both normal and renally impaired groups; the increases were statistically significant in the renally impaired group (n = 14). Prazosin was associated with small decreases in both measures in both groups. One patient died of myocardial infarction during the placebo run-in. There were no other serious adverse events. Four patients reported dizziness (2 with each drug). We conclude that with appropriate dose titration, bunazosin retard is well tolerated and preserves renal blood flow when used to treat hypertension in patients with renal insufficiency.
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PMID:Renal haemodynamic effects of bunazosin retard and prazosin in mild to moderately hypertensive patients with normal or moderately impaired renal function. 797 85


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