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Reflex control of circulation and angiotensin converting enzyme inhibition in man
G Mancia1, C Giannattasio, G Grassi
1Cattedra di Semeiotica Medica e Istituto di Clinica Medica, Università di Milano, Italy.
Insights
Angiotensin converting enzyme (ACE) inhibitors like captopril may affect blood pressure regulation. While ACE inhibitors reduce forearm vasoconstriction, they preserve arterial baroreflex function, preventing orthostatic hypotension.
Area of Science:
- Cardiovascular Physiology
- Pharmacology
- Hypertension Research
Background:
- Angiotensin II facilitates sympathetic cardiovascular responses, potentially enhancing antihypertensive effects of ACE inhibitors.
- However, inhibiting angiotensin II may disrupt essential reflexes for blood pressure homeostasis.
Purpose of the Study:
- To investigate the impact of captopril on reflex cardiovascular control in essential hypertension.
- To determine if ACE inhibition affects cardiopulmonary and arterial baroreflexes.
Main Methods:
- Forearm vasomotor responses to cardiopulmonary receptor deactivation (lower body negative pressure) were measured before and after captopril.
- Arterial baroreflex function was assessed using vasoactive drug and neck chamber techniques.
Main Results:
- Captopril administration reduced forearm vasoconstriction in response to cardiopulmonary receptor deactivation.
- The increase in plasma renin activity and arterial baroreflex function (heart rate and blood pressure modulation) remained unchanged or improved.
Conclusions:
- ACE inhibition with captopril may adversely affect some reflex controls of circulation.
- Preservation of arterial baroreflex function likely prevents orthostatic hypotension during chronic ACE inhibitor treatment.
Abstract:
Removal of the facilitating effect of angiotensin II on sympathetic cardiovascular influences may enhance the antihypertensive effect of angiotensin converting enzyme (ACE) inhibitors but may also disturb reflexes involved in blood pressure homeostasis. To test this hypothesis in essential hypertensive subjects, the forearm vasomotor response to cardiopulmonary receptor deactivation (lower body negative pressure) was studied before and after acute or prolonged administration of captopril at doses capable of lowering blood pressure and blocking the formation of angiotensin II. After either acute or prolonged captopril administration there was less response (i.e. forearm vasoconstriction) than in the no-drug state. However, in the same subjects, another reflex response to cardiopulmonary receptor deactivation, the increase in plasma renin activity, was not blunted by the drug. Furthermore, the other major reflex responsible for blood pressure homeostasis, the arterial baroreflex, was left unchanged or was even favoured by administration of clinically effective doses of captopril. This finding applied to both the heart rate and the blood pressure modulating ability of the reflex (vasoactive drug and neck chamber techniques, respectively). Thus, reflex control of circulation may be adversely affected by ACE inhibition. However, this does not include all reflex targets and at least one major reflex is preserved following this pharmacological intervention. This may explain why our patients showed no orthostatic hypotension during chronic treatment with ACE inhibitors.