Role of renal nerves in experimental hypertension: evaluation of neurogenic mechanisms.

To evaluate neurogenic mechanisms underlying variations in arterial pressure associated with removal of baroreflexes, renal sympathetic nerve activity (RSNA) was recorded in conscious unrestrained rats 1 day and 14 days following sinoaortic deafferentation (SAD) or sham operation. Fluctuations in RSNA and heart rate (HR) were correlated stastistically with moment to moment changes in pressure. One day and 14 days after SAD, the lability of mean arterial pressure (MAP) was increased, whereas the lability of RSNA and HR were reduced at 1 day and unchanged at 14 days. Arterial pressure and RSNA were negatively correlated in sham rats, however in rats with SAD negative correlations were virtually absent and positive correlations appeared only infrequently. These results indicate that SAD reduces variability of both RSNA and HR and that lability of arterial pressure appears to not be driven by variations in sympathetic discharge. To examine the central origins of RSNA in anesthetized rats we blocked neuronal transmission in two vasomotor regions of rostral medulla, rostral ventrolateral medulla (RVLM) and rostral ventromedial medulla (RVMM) using bilateral microinjections of lidocaine. Blockade of either or both RVLM and RVMM produced an equivalent marked reduction in arterial pressure but reduced RSNA to only 40% of control. Ganglionic blockade had little additional effect on arterial pressure but abolished the residual RSNA. These findings suggest that a substantial fraction of RSNA may be non-vasomotor in function and that this activity may originate from spinal sites or from supraspinal sites other than RVLM or RVMM.