The acute administration of the beta-adrenoceptor antagonists propranolol (80 mg) and atenolol (50 mg) on baroreflex function were investigated in healthy volunteers. Two h after administration both propranolol and atenolol significantly prolonged the supine R-R interval (1126, 1128 ms respectively) compared to placebo (1012 ms); systolic arterial pressure also fell (102.9, 102.0 mm Hg respectively) compared to placebo (112.6 mm Hg). Baroreflex function, assessed using glyceryl trinitrate to deactivate the baroreceptors was unchanged by these drugs compared to placebo. Baroreflex sensitivity (slope of the linear regression line relating R-R interval to systolic blood pressure) using phenylephrine to activate the baroreceptors, was also unchanged (17.2, 17.9 ms/mm Hg respectively) compared to placebo (19.9 ms/mm Hg). However both regression lines were shifted (p less than 0.05) to the left compared to placebo.
Methoxamine and alpha-methyl-noradrenaline were administered to six healthy male subjects on separate days as rapid bolus injections until blood pressure increased by approximately 30 mmHg; Valsalva's Manoeuvre was carried out on each occasion. Propranolol (80 mg) or placebo was administered (random order, double-blind, weekly intervals) and the observations were repeated after 2 h. Baroreceptor sensitivity (delta R-R interval ms/mmHg systolic BP) was less (p less than 0.05) with alpha-methyl-noradrenaline than methoxamine. Propranolol abolished the differences in baroreceptor-mediated bradycardia following alpha-methyl-noradrenaline and methoxamine, and shifted the baroreceptor sensitivity regression lines (p less than 0.05) to the left. During the release phase of Valsalva's Manoeuvre baroreceptor sensitivity was increased following propranolol. The smaller baroreceptor-mediated bradycardia response observed with alpha-methyl-noradrenaline does not support the hypothesis that pre-synaptic alpha-adrenoreceptors have a physiological role in the modulation of baroreceptor function in man, and may be due to alpha-methyl-noradrenaline having beta 1-agonist activity.
1. The effects of the acute and chronic administration of the alpha 1‐ adrenoceptor antagonist alfuzosin (5 mg twice daily for 7 days) on baroreflex function, physiological tremor and sedation (visual analogue scale) were investigated in six healthy volunteers. 2. Phenylephrine‐ systolic pressure dose‐response curves were shifted (P less than 0.05) to the right by alfuzosin compared with placebo on day 1, and on day 8 prior to the administration of alfuzosin indicating significant alpha‐ adrenoceptor blockade over 24 h with 5 mg twice daily administration. 3. Baroreflex sensitivity (delta R‐R ms mmHg‐1 systolic arterial pressure) was reduced (P less than 0.05) by alfuzosin compared with placebo on day 1 (13.8 +/‐ 2.6 vs 20.6 +/‐ 3.6 ms mmHg‐1) and on day 8 (13.4 +/‐ 1.7 vs 21.1 +/‐ 2.7 ms mmHg‐1). 4. Maximum power (microV2) or frequency (Hz) of physiological tremor did not change 2 h after alfuzosin administration on day 1 (13.7 +/‐ 4.4 microV2, 9.2 +/‐ 0.3 Hz) or day 8 (11.5 +/‐ 4.3 microV2, 10.0 +/‐ 0.4 Hz) compared with placebo on day 1 (16.9 +/‐ 7.5 microV2, 10.0 +/‐ 0.4 Hz) and day 8 (17.3 +/‐ 5.7 microV2, 10.2 +/‐ 0.8 Hz). 5. Alfuzosin 5 mg twice daily did not cause sedation on day 1 or day 8. 6. In conclusion the reduction in baroreflex sensitivity with the alpha‐adrenoceptor antagonist alfuzosin may contribute to its antihypertensive activity in reducing the reflex tachycardia associated with its hypotensive action.
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