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Research Article Free access | 10.1172/JCI113613

Cardiac and peripheral circulatory responses to angiotension and vasopressin in dogs.

R W Lee, S Standaert, L D Lancaster, D Buckley, and S Goldman

Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.

Find articles by Lee, R. in: PubMed | Google Scholar

Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.

Find articles by Standaert, S. in: PubMed | Google Scholar

Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.

Find articles by Lancaster, L. in: PubMed | Google Scholar

Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.

Find articles by Buckley, D. in: PubMed | Google Scholar

Department of Internal Medicine, Tucson Veterans Administration Medical Center, Arizona 85723.

Find articles by Goldman, S. in: PubMed | Google Scholar

Published August 1, 1988 - More info

Published in Volume 82, Issue 2 on August 1, 1988
J Clin Invest. 1988;82(2):413–419. https://doi.org/10.1172/JCI113613.
© 1988 The American Society for Clinical Investigation
Published August 1, 1988 - Version history
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Abstract

To determine the cardiac and peripheral circulatory responses to changes in afterload with angiotension and vasopressin, we increased mean aortic pressure 25% and 50% above control in splenectomized and ganglion-blocked dogs. We compared these responses to similar mechanical increases in aortic pressure produced by partial balloon occlusion of the descending aorta. With 25% or 50% increases in aortic pressure, angiotensin, vasopressin, and balloon inflation produced no changes in heart rate, right atrial, and mean pulmonary artery pressures. At 25% increase in aortic pressure, cardiac output was maintained with angiotensin and balloon occlusion but decreased with vasopressin. At 50% increase in aortic pressure, cardiac output was maintained with only balloon occlusion and decreased with both angiotensin and vasopressin. Whenever cardiac output fell, central blood volume did not increase as after-load increased. These changes in preload can be explained by alterations in the venous circulation. Vasopressin did not alter venous compliance or unstressed vascular volume but increased resistance to venous return. Angiotensin also increased resistance to venous return but decreased venous compliance and did not change unstressed vascular volume. Balloon occlusion had no effects on these parameters. We conclude that: (a) angiotensin caused significant venoconstriction resulting in maintenance of cardiac output at 25% but not 50% increase in aortic pressure; (b) vasopressin increased the resistance to venous return without venoconstriction; this resulted in a fall in cardiac output even with a 25% increase in aortic pressure; and (c) the effects of the agents on the venous circulation were independent of the mechanical effects of a pressure increase in the arterial circulation.

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