To examine whether cardiopulmonary receptors participate in the reflex control of coronary vascular resistance, systemic and coronary hemodynamics were assessed before and during -10 mm Hg lower body negative pressure in eight normal subjects and eight hypertensive patients with left ventricular hypertrophy. In both study groups, lower body negative pressure induced a significant decrease in right atrial pressure, left ventricular filling pressure and cardiac output, an increase in systemic vascular resistance and no change in mean arterial pressure and heart rate. In normal subjects, there was also a significant increase in plasma norepinephrine concentration (from 294 ± 39 to 421 ± 47 pg/ml, p <0.01). This increase was accompanied by a reduction in coronary blood flow, assessed by the continuous thermodilution method (from 101 ± 5 to 79 ± 4 ml/min, p <0.05). An increase in coronary vascular resistance (from 0.865 ± 0.1 to 1.107 ± 0.1 mm Hg/ml per min, p <0.05) and in myocardial oxygen consumption was detected in normal subjects during cardiopulmonary baroreceptor unloading. In contrast, in hypertensive patients, -10 mm Hg lower body negative pressure failed to induce any change in plasma norepinephrine, coronary blood flow or vascular resistance. Intravenous propranolol administration caused no significant change in the systemic hemodynamic response to -10 mm Hg lower body negative pressure in either study group, but it did abolish the decrease in coronary flow and the increase in plasma norepinephrine, coronary vascular resistance and myocardial oxygen consumption observed in normal subjects in control conditions. Finally, propranolol did not modify the systemic and coronary hemodynamic responses either to lower body negative pressure in hypertensive patients or to a 60 mm Hg increase in neck tissue pressure in both groups of subjects. These results suggest that cardiopulmonary baroreceptors participate in the reflex control of coronary vascular tone in normal subjects and that this response is abolished in hypertensive patients with left ventricular hypertrophy as a result of an altered cardiopulmonary receptor function.
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