Abstract

The aim of the present study was to investigate how loading of cardiopulmonary baroreceptors induced by water immersion (WI) modifies baroreflex control of renal sympathetic nerve activity (RSNA) in conscious dogs. Nine dogs were chronically instrumented for measuring carotid sinus nerve activity (CSNA), RSNA, carotid arterial (Pca), and central venous (Pcv) pressures. The stimulus-response relationships of Pca-CSNA and Pca-RSNA were determined simultaneously in the same dog by changing Pca using rapid intravenous infusions vasoactive drugs during pre-WI and WI. WI increased central venous pressure significantly (P < 0.05) by 10.4 mmHg. WI shifted the Pca-RSNA curve acutely leftward compared with the pre-WI period, which was associated with significant (P < 0.05) decreases in the saturation pressure by 39.0 mmHg and operating range by 43.1 mmHg. WI relocated the operating pressure to near the saturation pressure, where the gain was low. The Pca-CSNA curve obtained during WI was identical to that obtained during pre-WI period. These results suggest that the shift in baroreflex control of RSNA could be attributed to the inhibitory influence of the cardiopulmonary mechanoreceptor loading and not by the resetting of carotid baroreceptors per se.

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