Faculty Collaboration Database

Vasoconstriction during volume expansion is independent of central control. Hypertension 1990 Jun;15(6 Pt 2):712-7

Date

06/01/1990

Pubmed ID

2351426

DOI

10.1161/01.hyp.15.6.712

Scopus ID

2-s2.0-0025370609 (requires institutional sign-in at Scopus site)   6 Citations

Abstract

We have previously demonstrated that, in the absence of the rapid acting neural and hormonal controllers of blood pressure, an acute blood volume expansion of only 5% in unanesthetized rats caused an increase in total peripheral resistance (TPR) of 22%. Either whole body autoregulation or the release of a putative ouabainlike factor from the central nervous system (CNS) could have explained these responses. The purpose of the present study was to investigate the possible contribution of a centrally released ouabainlike factor to the vasoconstriction response observed during volume expansion. Because the anteroventral third ventricle (AV3V) region is proposed to be important in the control of this putative factor, we compared the hemodynamic responses to blood volume expansion in rats with AV3V lesions (n = 6), sham lesions (n = 6), and total CNS ablation (n = 6). The results of our studies showed that neither AV3V lesion nor CNS ablation reduced the increases of total peripheral resistance seen with blood volume expansion. We conclude that centrally released factors are not required for vasoconstriction in response to acute volume expansion and that regional autoregulatory mechanisms result in a net increase of systemic vascular resistance (i.e., whole body autoregulation).

Author List

Hinojosa-Laborde C, Thunhorst RL, Cowley AW Jr

Author

Allen W. Cowley Jr PhD Professor in the Physiology department at Medical College of Wisconsin

MESH terms used to index this publication - Major topics in bold

Animals
Blood Circulation
Blood Pressure
Brain
Cerebral Ventricles
Denervation
Hemodynamics
Male
Plasma Substitutes
Rats
Rats, Inbred Strains
Spinal Cord
Vasoconstriction