In young Wistar-Kyoto rats (WKY) and spontaneously hypertensive rats (SHR) with or without chronic sinoaortic denervation (SAD), we evaluated the effects of low, regular, and high dietary sodium intake (L-Na, R-Na, and H-Na, respectively) from 4 to 8 wk of age on cardiopulmonary baroreflex function, which was assessed by changes in renal sympathetic nerve activity (RSNA) and heart rate (HR) in response to acute volume expansion. In intact SHR H-Na increased blood pressure (BP), whereas L-Na decreased BP. No changes were observed in intact WKY. The gain of the cardiopulmonary baroreflex control of both HR and RSNA was significantly attenuated in SHR vs. WKY on R-Na. In both SHR and WKY, L-Na had no effects on the gain of RSNA and HR responses. In both strains, H-Na did not affect the gain of HR but attenuated the gain of the RSNA response. H-Na attenuated the gain of RSNA response more in SHR with SAD vs. intact SHR (52 vs. 69% of corresponding R-Na control) but less in WKY with SAD vs. intact WKY (80 vs. 71% of corresponding R-Na control). These data indicate that in SHR, H-Na further desensitizes the already impaired cardiopulmonary baroreflex control of RSNA. After SAD, this attenuation is more prominent in SHR but becomes less prominent in WKY. High sodium intake, therefore, modulates the interaction between the arterial and cardiopulmonary baroreflexes in the control of RSNA oppositely in WKY vs. SHR.
Tonic and reflex control of renal sympathetic nerve activity are altered by a discrete increase in sodium intake in renovascular hypertensive rats