Why the study?
Does captopril exhibit parasympathetic activity affecting hemodynamics in normotensive subjects?
Does captopril exhibit parasympathetic activity affecting hemodynamics in normotensive subjects?
Captopril demonstrates parasympathetic activity that may contribute to its hemodynamic profile, such as lowering blood pressure without causing reflex tachycardia.
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Captopril may lower BP without reflex tachycardia via parasympathetic effects; hypothesis-generating in normotensives and requires confirmation in patients.
Captopril (50 mg orally) produced a significant fall in systolic and diastolic blood pressure in six normotensive sodium replete subjects, without a rise in heart rate. On captopril, there was no change in the expected normal increase in heart rate on standing. Supine plasma noradrenaline was not reduced by captopril and normal postural increases were maintained. Atropine (0.04 mg/kg i.v.) reduced the difference in blood pressure change between captopril and placebo. Facial immersion in water produced a bradycardia. This change was abolished by atropine and attenuated both by captopril and edrophonium (10 mg i.v.), a cholinesterase inhibitor. Lying down after 6 min standing produced an immediate transient tachycardia, which was abolished by atropine and attenuated by captopril. Blood pressure and heart rate rose after a cold pressor test on both captopril and placebo. The tachycardia during the Valsalva manoeuvre was inhibited by edrophonium and to a lesser extent by captopril. The effects of captopril and edrophonium were additive. Parasympathetic activity of captopril may contribute to its haemodynamic profile.
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Campbell et al. (1985) studied this question.
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