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Am J Physiol Heart Circ Physiol 274: H1121-H1131, 1998;
0363-6135/98 $5.00
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Vol. 274, Issue 4, H1121-H1131, April 1998

Reduction in arterial compliance alters carotid baroreflex control of cardiac output in a model of hypertension

Jeffrey T. Potts1, Kelly P. McKeown2, and Artin A. Shoukas2

1 Department of Physiology, Harry S. Moss Heart Center, University of Texas Southwestern Medical Center, Dallas, Texas 75235; and 2 Department of Biomedical Engineering, The Johns Hopkins University School of Medicine, Baltimore, Maryland 21205

Baroreflex regulation of cardiac output is determined by the performance of the heart as well as the available blood flow returning to the heart (i.e., venous return). We hypothesized that a decrease in arterial compliance (Ca) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Baroreflex control of systemic arterial pressure (Pa), central venous pressure (Pv), heart rate, cardiac output (CO), and peripheral vascular resistance (R) were determined during bilateral carotid occlusion (BCO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawley (normotensive, NT) rats. Ca was determined from the rate of arterial pressure decay when CO was transiently stopped, and the VR curve was obtained during graded inflation of a vascular balloon positioned in the right atrium. The inverse slope of the VR curve was used as an index of the resistance to venous return (RVR). The baseline slope of the VR curve was -50.5 ± 3.3 vs. -35.5 ± 2.6 ml · kg-1 · min-1 · mmHg-1 in NT vs. HT, respectively (P < 0.05). Control values of Pa (96 ± 5 vs. 124 ± 8 mmHg) and R [0.43 ± 0.04 vs. 0.80 ± 0.07 peripheral resistance units (PRU)] were reduced in NT, whereas Ca (0.062 ± 0010 vs. 0.036 ± 0.003 ml · kg-1 · mmHg-1) was elevated in NT vs. HT, respectively (P < 0.05). Analysis of the pressure dependence of Ca demonstrated that Ca was a nonlinear function of Pa, and the exponential decay constant for the Ca-Pa relationship was reduced in HT (0.0055 ± 0.0012 vs. 0.0012 ± 0.0002 min, NT vs. HT, P < 0.05). Baroreflex activation by BCO significantly increased Pa (Delta Pa, 20 ± 4 vs. 28 ± 3 mmHg) and R (Delta R, 0.16 ± 0.04 vs. 0.24 ± 0.06 PRU) in NT vs. HT, respectively. However, BCO significantly decreased CO in NT but not HT (Delta CO, -24 ± 5 vs. -4 ± 6 ml · kg-1 · min-1, P < 0.05). In NT, RVR was increased 39 ± 9% during BCO (P < 0.05), whereas RVR increased 8 ± 3% in HT (P = NS). From these findings, we conclude that the difference in baroreflex control of CO is mediated, in part, by the reduction in Ca, which minimized the baroreflex-evoked increase in RVR.

blood volume distribution; vascular capacitance; sympathetic nervous system


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