Hemodynamic effects of angiotensin, norepinephrine, and bradykinin continuously measured in unanesthetized dogs

¹ Research Division, The Cleveland Clinic Foundation; and The Frank E. Bunts Educational Institute, Cleveland, Ohio

Cardiac output, arterial pressure, heart rate and the derived functions, peripheral resistance and stroke volume, were registered continuously from intact, unanesthetized, unrestrained dogs. Isoleucyl⁵- or valyl⁵-angiotensin octapeptide caused output, heart rate and stroke volume to fall sharply when peripheral resistance rose. When infused for an hour, systolic and diastolic pressure remained elevated with unchanged infusion rate. Heart rate decreased in most animals, stroke volume and cardiac output fell, while peripheral resistance rose. Pentobarbital anesthesia increased somewhat the pressor response and decreased the bradycardia. Norepinephrine elicited, first, an abrupt rise in pressure and peripheral resistance, slight rise in heart rate and stroke volume. Arterial pressure then tended to stabilize, followed by a slow decrease associated with continued depression of cardiac output. Bradykinin caused fall in pressure, partial recovery, then further fall. Heart rate slowed, then rose. Cardiac output rose sharply during the initial fall in arterial pressure and remained elevated during the hypotensive response. Stroke volume was reduced during the initial fall but was reduced less during the rest of the response. Peripheral resistance was decreased sharply.

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