Key result
Intravenous angiotensin II in conscious sheep produced a dose-dependent tachycardia via a central reduction in vagal tone, an effect normally antagonized by the baroreceptor reflex.
Why the study?
Does intravenous angiotensin II affect heart rate in conscious sheep when its pressor action is antagonized?
Does intravenous angiotensin II affect heart rate in conscious sheep when its pressor action is antagonized?
Intravenous angiotensin II causes a central, dose-dependent reduction in vagal tone leading to tachycardia when blood pressure is not elevated.
Prompts reevaluation of angiotensin II's autonomic actions beyond pressor effects; leaves open translation to human heart rate control.
Intravenous infusions of angiotensin II were given to conscious sheep. During these infusions, the pressor action of angiotensin was antagonized by concomitant infusion of sodium nitroprusside. Under these conditions, angiotensin produced a dose-dependent tachycardia. This dose-dependent tachycardia was not affected by propranolol and therefore it was not due to an action of angiotensin on sympathoadrenal mechanisms. The dose-dependent tachycardia was reduced by atropine, and abolished by increases in systolic pressure. We conclude that iv infusions of angiotensin cause a central, dose-dependent reduction in vagal tone. This action is normally antagonized by the baroreceptor reflex response to the hypertensive action of angiotensin. Therefore, in those conditions in which endogenous angiotensin production is increased and blood pressure is not elevated (e.g., sodium deficiency and pregnancy), angiotensin may influence heart rate.
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Lee et al. (1980) studied Conscious sheep. Intravenous angiotensin II was evaluated on Heart rate (tachycardia). Intravenous angiotensin II in conscious sheep produced a dose-dependent tachycardia via a central reduction in vagal tone, an effect normally antagonized by the baroreceptor reflex.
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