MUSCLE CHEMOREFLEX-INDUCED INCREASES IN RIGHT ATRIAL PRESSURE

When oxygen delivery to active muscle is too low for the ongoing rate of metabolism, metabolites accumulate and stimulate sensory nerves wit hin the muscle leading to sympathetic activation (muscle chemoreflex). To date, studies on this reflex have focused primarily on its ability to increase arterial pressure or on the activity of the nerves that m ediate this response. Clearly, a rise in cardiac output (CO) constitut es an important adjustment, because it increases the total blood flow available to be distributed among organs competing for flow However, i ncrements in heart rate and contractility provide limited means of rai sing CO because of the inverse relationship that exists between CO and right atrial pressure (RAP) in the intact circulation. Our goal was t o test whether muscle chemoreflex activation, achieved via graded redu ctions in hindlimb blood flow by partial vascular occlusion, elicits p eripheral vascular adjustments that raise RAP. In four conscious dogs exercising on a treadmill at 3.2 km/h 0% grade, RAP was well maintaine d during reflex activation despite increases in CO and arterial pressu re that are expected to reduce RAP. Thus peripheral vascular adjustmen ts elicited by the reflex successfully defend RAP in a setting where i t would otherwise fall. To isolate the effects of the reflex on RAP, C O was maintained constant by ventricular pacing in conjunction with be ta(1)-adrenergic blockade with atenolol. When the reflex was activated by reducing hindlimb blood flow from 0.6 to 0.3 l/min, RAP rose from 5.1 +/- 0.8 to 7.4 +/- 0.4 mmHg (P < 0.05) despite continued large (40 mmHg) increases in arterial pressure. During heavier exercise (6.4 km /h 10% grade) in five dogs with normal ventricular function, the refle x raised RAP from 5.7 +/- 0.9 to 6.6 +/- 0.8 mmHg (P < 0.05) despite i ncreases in CO and arterial pressure. We conclude that the muscle chem oreflex is capable of eliciting substantial increases in RAP.