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Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity In contrast to the reflex control of heart rate, reports on the baroreflex control of arterial pressure vascular resistance during II have not always been consistent. For example, it has been shown that II may attenuate reflex depressor vasodilator responses to arterial baroreceptor stimulation without altering the pressor vasoconstrictor response to bilateral carotid artery occlusion (7, 18, 24). Conversely, Goldstein et al. (8) reported that II augments reflex vasoconstrictor responses during carotid hypotension ‘but the reflex vasodilator responses to increased carotid sinus pressures remained unchanged. Thus, although the attenuation of baroreflex-mediated bradycardia by II has been confirmed, the influence of II on the baroreflex control in arterial pressure vascular resistance is still open to question, there are no data on the effect of II on the baroreflex-mediated tachycardia. Interpretation of reflex changes in arterial pressure vascular resistance after II may be difficult because of the direct vascular effects of ’I1 as well as its effects on neurotransmitter release (29). Therefore, the purpose of this study was to determine if II modulates baroreflex control of lumbar sympathetic nerve activity as well as heart rate during increases decreases in arterial pressure. We also examined possible mechanisms for the modulation of http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

Angiotensin II attenuates baroreflex control of heart rate and sympathetic activity

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Publisher
The American Physiological Society
Copyright
Copyright © 1984 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
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Abstract

In contrast to the reflex control of heart rate, reports on the baroreflex control of arterial pressure vascular resistance during II have not always been consistent. For example, it has been shown that II may attenuate reflex depressor vasodilator responses to arterial baroreceptor stimulation without altering the pressor vasoconstrictor response to bilateral carotid artery occlusion (7, 18, 24). Conversely, Goldstein et al. (8) reported that II augments reflex vasoconstrictor responses during carotid hypotension ‘but the reflex vasodilator responses to increased carotid sinus pressures remained unchanged. Thus, although the attenuation of baroreflex-mediated bradycardia by II has been confirmed, the influence of II on the baroreflex control in arterial pressure vascular resistance is still open to question, there are no data on the effect of II on the baroreflex-mediated tachycardia. Interpretation of reflex changes in arterial pressure vascular resistance after II may be difficult because of the direct vascular effects of ’I1 as well as its effects on neurotransmitter release (29). Therefore, the purpose of this study was to determine if II modulates baroreflex control of lumbar sympathetic nerve activity as well as heart rate during increases decreases in arterial pressure. We also examined possible mechanisms for the modulation of

Journal

AJP - Heart and Circulatory Physiology – The American Physiological Society

Published: Jan 1, 1984

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