Relative roles of vagal and sympathetic effector mechanisms in the baroreflex control of myocardial contractility in conscious rabbits

Abstract

The relative roles of vagal and sympathetic effector mechanisms in the baroreflex control of myocardial contractility have been assessed in the conscious normotensive and hypertensive rabbit. Graded increases in mean arterial pressure (MAP) were produced by inflation of a balloon occluder around the abdominal aorta. Stimulus response curves relating the change in MAP to the induced change in peak rate of change of left ventricular pressure (peak LV dP/dt) were produced when heart rate was allowed to change and when it was held constant by atrial pacing. These curves were repeated after sympathetic blockade with propranolol, vagal blockade with methylscopolamine and combined blockade with the two drugs together. Increase in MAP produced a reflex fall in peak LV dP/dt which was due to two components. There was a reflex negative inotropic effect which was independent of heart rate, occurring in animals in whom heart rate was held constant by atrial pacing, and there was also a reduction in peak LV dP/dt which was caused by the reflex bradycardia when the heart rate was allowed to change. Both sympathetic and vagal efferents contributed to the reflex fall in peak LV dP/dt seen after elevation of MAP, the sympathetic being primarily responsible for the direct negative inotropic effect and the vagus for the bradycardia and hence the secondary effects on peak LV dP/dt. The slope of the stimulus response curves relating the fall in peak LV dP/dt to the increase in MAP was similar in intact normotensive and hypertensive rabbits, both with and without atrial pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic central versus systemic blockade of AT1 receptors and cardiac dysfunction in rats post-myocardial infarction

“…Subsequently in protocol I, 5% dextrose was infused intravenously via the left jugular vein for two consecutive periods at 0.01 and 0.03 ml/100 g BW/s, each for 30 s. LV hemodynamics were recorded continuously for 5 min after the volume overload. Increases in LVEDP and decreases in dP/dt max in response to intravenous infusion of dextrose at these two rates were recorded and used to estimate cardiopulmonary baroreflex function (2,18).…”