Direct Recording of Cardiac and Renal Sympathetic Nerve Activity Shows Differential Control in Renovascular Hypertension

There is increasing evidence that hypertension is initiated and maintained by elevated sympathetic tone. Increased sympathetic drive to the heart is linked to cardiac hypertrophy in hypertension and worsens prognosis. However, cardiac sympathetic nerve activity (SNA) has not previously been directly recorded in hypertension. We hypothesized that directly recorded cardiac SNA levels would be elevated during hypertension and that baroreflex control of cardiac SNA would be impaired during hypertension. Adult ewes either underwent unilateral renal artery clipping (n=12) or sham surgery (n=15). Two weeks later, electrodes were placed in the contralateral renal and cardiac nerves to record SNA. Baseline levels of SNA and baroreflex control of heart rate and sympathetic drive were examined. Unilateral renal artery clipping induced hypertension (mean arterial pressure 109 +/- 2 versus 91 +/- 3 mm Hg in shams; P<0.001). The heart rate baroreflex curve was shifted rightward but remained intact. In the hypertensive group, cardiac sympathetic burst incidence (bursts/100 beats) was increased (39 +/- 14 versus 25 +/- 9 in normotensives; P<0.05), whereas renal sympathetic burst incidence was decreased (69 +/- 20 versus 93 +/- 8 in normotensives; P<0.01). The renal sympathetic baroreflex curve was shifted rightward and showed increased gain, but there was no change in the cardiac sympathetic baroreflex gain. Renovascular hypertension is associated with differential control of cardiac and renal SNA; baseline cardiac SNA is increased, whereas renal SNA is decreased.