Continuous measurement of renal cortical blood flow and renal arterial blood flow during stimulation of the renal nerve.

Stimulation of the renal sympathetic nerve in young pigs with biphasic pulses of current (3 mA, 800 microseconds per phase, 5, 10 and 50 Hz) produced decreases in arterial and cortical blood flow in the kidney, with the greatest decreases occurring at the highest stimulus frequencies. The decrease in cortical flow lagged that in arterial flow by 1.53-1.99 s; the delay increased with decreasing frequency but was unaffected by captopril, an angiotensin-converting enzyme-blocking agent. This result was consistent with the hypothesis that stimulation of the sympathetic nerve causes constriction first in the afferent arteriole and then in the efferent arteriole. Systemic arterial pressure increased during stimulation of the nerve; the increase was greater in intact nerves than in nerves that had been crushed proximal to the point of the stimulus, indicating that pigs do have renal afferent nerves. Pressure increased after the stimulus ended, but the increase abated or changed to a decrease after administration of captopril. The changes in flow were unaffected by administration of captopril, but were markedly reduced by the blocking agent labetalol (renal arterial flow, 77 +/- 14 per cent; cortical flow, 70 +/- 12 per cent). Thus, the observed changes in flow resulted from direct stimulation of the sympathetic nerves and not from stimulation of the renin-angiotensin system, which affects the pressure response after the stimulus.