Effects of celiprolol on reflex control of the cardiovascular system in essential hypertension

We have previously shown that baroreceptor control of the cardiovascular system and the cardiopulmonary receptor control of peripheral circulation are preserved or only moderately reduced during antihypertensive treatment with acebutolol or nadolol, which indicates that treatment with beta blockers with or without intrinsic sympathomimetic activity does not impair fundamental neural mechanisms involved in circulatory homeostasis. In the present study we have investigated the reflex control of circulation before and during antihypertensive treatment with celiprolol, which, in addition to its beta-blocking action, has vasodilator properties that may stem from interference with neural cardiovascular control. In six essential hypertensive subjects we measured blood pressure (intraarterial catheter), heart rate (ECG recording), central venous pressure (right atrial catheter), and forearm blood flow and resistance (plethysmography) before and during alterations in the activity of the arterial baroreceptors obtained by means of lower body suction and passive leg raising. The study was performed before and after 5-7 days of oral administration of celiprolol at 200-400 mg once a day. Compared to the values obtained in the control, condition celiprolol caused a reduction in blood pressure, a slight change in heart rate, and an increase in forearm blood flow, which indicated the occurrence of a clear-cut forearm vasodilatation. The heart rate responses to arterial baroreceptor manipulation were unchanged by celiprolol which reset the carotid baroreflex so that its tonic restraint on blood pressure increased despite the hypotension induced by the drug. The inhibitory restraint tonically exerted by the cardiopulmonary receptors on peripheral circulation was also increased by celiprolol.(ABSTRACT TRUNCATED AT 250 WORDS

ACE INHIBITION ATTENUATES SYMPATHETIC CORONARY VASOCONSTRICTION IN PATIENTS WITH CORONARY-ARTERY DISEASE

Background. In humans, angiotensin converting enzyme (ACE) inhibition attenuates the vasoconstriction induced by sympathetic stimulation in a number of peripheral districts. Whether this is also the case in the coronary circulation is unknown, however. Methods and Results. In nine normotensive patients with angiographically assessed coronary atherosclerosis, we measured the changes in mean arterial pressure (intra-arterial catheter), heart rate, rate-pressure product (RPP), coronary sinus blood flow (CBF, thermodilution method), and coronary vascular resistance (CVR, ratio between mean arterial pressure and CBF) induced by the cold pressor test (CPT, 2 minutes) and diving (30 seconds), i.e., two stimuli eliciting a sympathetic coronary vasoconstriction. The measurements were performed in the control condition and 30 minutes after captopril 25 mg p.o. In the control condition, CPT caused an increase in mean arterial pressure and heart rate. Despite the increase in RPP (+20.7+/-3.2%, p Conclusions. ACE inhibition attenuates sympathetic coronary vasoconstriction in patients with coronary artery disease. This is probably due to removal of the facilitating influence of angiotensin II on sympathetic modulation of coronary vasomotor tone