Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011570 (depression)
172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the effects of alpha 1-adrenoceptor blockade with indoramin on exercise tolerance in 15 patients with chronic stable angina using a double-blind crossover protocol. Thirteen patients had been receiving beta-adrenoceptor blocking drugs and nitrates. The therapy of these patients was continued unchanged throughout the study. Indoramin, in a dose of 25 mg three times daily, prolonged exercise duration by 17% (p less than 0.01) and increased oxygen consumption during exercise by 21% (p less than 0.01), while the maximal double product was unchanged. This increase in exercise capacity was associated with significant attenuation in ST segment depression during exercise. To investigate the mechanism of this antianginal effect, we studied the effects of indoramin (0.2 mg/kg i.v.) on coronary and systemic haemodynamics in a further 11 male patients with chronic stable angina who were receiving beta-adrenoceptor blocking drugs. Measurements were obtained during sinus rhythm and during atrial pacing from 100 beats/min, incremented by 20 beats/min at intervals of 3 min until the onset of angina. Indoramin had no effect on resting heart rate (64 +/- 2 vs. 67 +/- 2 beats/min), but did prolong pacing time to angina (7.4 +/- 0.7 vs. 5.4 +/- 0.5 min; p less than 0.005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antianginal and haemodynamic effects of alpha 1-adrenoceptor blockade. 242 88

Several mechanisms have been suggested for the absence of reflex tachycardia in response to the hypotensive effect of the selective alpha 1-adrenoceptor antagonist indoramin, including, in animals, membrane-stabilising activity, prolongation of repolarisation time, and reduction in baroreflex sensitivity. The present study investigated the effect of acute and chronic oral administration of indoramin (50 mg daily for 8 days) on baroreflex sensitivity in six healthy male volunteers. Baroreflex function was measured by determining the relationship between systolic blood pressure (SBP) and R-R interval following intravenous administration of phenylephrine. Indoramin shifted (p less than 0.05) the phenylephrine dose-response curve to the right on days 1 and 8 compared with placebo. Baroreflex sensitivity [R-R (ms)/SBP (mm Hg)] was reduced (p less than 0.05) by indoramin on day 1 compared with placebo (18.3 +/- 1.3 vs. 11.2 +/- 2.2 ms/mm Hg), and on day 8 compared with pretreatment values (18.3 +/- 2.8 vs. 10.8 +/- 1.8 ms/mm Hg). Acute but not chronic administration of indoramin caused (p less than 0.05) sedation; tremor tended to increase with chronic administration. It is suggested that depression of baroreflex sensitivity by indoramin may explain, in part, the lack of reflex tachycardia associated with its antihypertensive effect.
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PMID:Effect of acute and chronic indoramin administration on baroreflex function and tremor in humans. 245 20