Sympathetically mediated increases in cardiac output, not restraint of peripheral vasodilation, contribute to blood pressure maintenance during hyperinsulinemia

Author:

Limberg Jacqueline K.12,Smith James A.1,Soares Rogerio N.3ORCID,Harper Jennifer L.1,Houghton Keeley N.1,Jacob Dain W.1,Mozer Michael T.2,Grunewald Zachary I.13,Johnson Blair D.24ORCID,Curry Timothy B.2,Baynard Tracy5,Manrique-Acevedo Camila367,Padilla Jaume13

Affiliation:

1. Department of Nutrition and Exercise Physiology, University of Missouri, Columbia, Missouri

2. Department of Anesthesia and Perioperative Medicine, Mayo Clinic, Rochester, Minnesota

3. Dalton Cardiovascular Research Center, University of Missouri, Columbia, Missouri

4. Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, New York

5. Integrative Physiology Laboratory, University of Illinois at Chicago, Chicago, Illinois

6. Division of Endocrinology, Diabetes and Metabolism, Department of Medicine, University of Missouri, Columbia, Missouri

7. Research Services, Harry S. Truman Memorial Veterans Hospital, Columbia, Missouri

Abstract

We examined the role of sympathetic activation in restraining vasodilatory responses to hyperinsulinemia and sustaining blood pressure in healthy adults. Data are reported from two separate experimental protocols in humans and one experimental protocol in isolated arteries from mice. Contrary to our hypothesis, the present findings support the idea that during hyperinsulinemia, a sympathetically mediated increase in cardiac output, rather than restraint of peripheral vasodilation, is the principal contributor to the maintenance of systemic blood pressure.

Funder

HHS | National Institutes of Health

University of Missouri

American Heart Association

Publisher

American Physiological Society

Subject

Physiology (medical),Cardiology and Cardiovascular Medicine,Physiology

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