Evidence for a physiological role of pulmonary arterial baroreceptors in sympathetic neural activation in healthy humans

Abstract

In animal models, distension of baroreceptors located in the pulmonary artery induces a reflex increase in sympathetic outflow; however, this has not been examined in humans. Therefore, we investigated whether reductions in pulmonary arterial pressure influenced sympathetic outflow and baroreflex control of muscle sympathetic nerve activity (MSNA). Healthy lowlanders (n=13; 5 females) were studied 4-8 days following arrival at high-altitude (4383m; Cerro de Pasco, Peru), a setting that increases both pulmonary arterial pressure and sympathetic outflow. MSNA (microneurography) and blood pressure (BP; photoplethysmography) were measured continuously during 1) ambient air breathing (Amb) and 2) a six-minute inhalation of the vasodilator nitric oxide (iNO; 40ppm in 21% O2), to selectively lower pulmonary arterial pressure. A modified Oxford test was performed under both conditions. Pulmonary artery systolic pressure (PASP) was determined using Doppler echocardiography. iNO reduced PASP (24±3 vs 32±5 mmHg; P < 0.001) compared to Amb, without changing heart rate (P= 0.6) or vascular-sympathetic baroreflex gain (P = 0.85). In conclusion, unloading of pulmonary arterial baroreceptors reduced basal sympathetic outflow to the skeletal muscle vasculature and reset vascular-sympathetic baroreflex control of MSNA downward and leftward in healthy humans at high-altitude. These data suggest the existence of a lesser-known reflex input involved in sympathetic activation in humans.