REDUCTION IN ARTERIAL COMPLIANCE ALTERS CAROTID BAROREFLEX CONTROL OFCARDIAC-OUTPUT IN A MODEL OF HYPERTENSION

Baroreflex regulation of cardiac output is determined by the performan ce of the heart as well as the available blood flow returning to the h eart (i.e., venous return). We hypothesized that a decrease in arteria l compliance (C-a) would affect carotid baroreflex control of cardiac output by altering the slope of the venous return curve (VR curve). Ba roreflex control of systemic arterial pressure (P-a), central venous p ressure (P-v), heart rate, cardiac output (GO), and peripheral vascula r resistance (R) were determined during bilateral carotid occlusion (B CO) in spontaneously hypertensive (hypertensive, HT) and Sprague-Dawle y (normotensive, NT) rats. C-a was determined from the rate of arteria l 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 ind ex 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 P-a (96 +/ - 5 vs. 124 +/- 8 mmHg) and R [0.43 +/- 0.04 vs. 0.80 +/- 0.07 periphe ral resistance units (PRU)] were reduced in NT, whereas C-a (0.062 +/- 0010 vs. 0.036 +/- 0.003 ml.kg(-1).mmHg(-1)) was elevated in NT vs. H T, respectively (P < 0.05). Analysis of the pressure dependence of C-a demonstrated that C-a was a nonlinear function of P-a, and the expone ntial decay constant for the C-a-P-a relationship was reduced in HT (0 .0055 +/- 0.0012 vs. 0.0012 +/- 0.0002 min, NT vs. HT, P < 0.05). Baro reflex activation by BCO significantly increased P-a (Delta P-a, 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 mediat ed, in part, by the reduction in C-a, which minimized the baroreflex-e voked increase in RVR.