Effects of hemorrhage on renal nerve activity in conscious dogs.

Abstract

We studied the effects of slow continuous hemorrhage (0.5 ml/kg per min) on measurements of arterial and left atrial pressures, and renal nerve activity in conscious dogs with all reflexes intact, or after sinoaortic baroreceptor denervation, cardiac denervation, or sinoaortic baroreceptor denervation plus vagal denervation. In intact dogs, mean arterial pressure remained relatively constant at 101 +/- 4 mm Hg until 20 +/- 4 ml/kg of hemorrhage, when renal nerve activity increased by 211 +/- 53%. At 39 +/- 2 ml/kg hemorrhage, mean arterial pressure fell by 48 +/- 3 mm Hg, and renal nerve activity returned to the prehemorrhage control level. Cardiac denervation did not affect the response of mean arterial pressure to hemorrhage, whereas, after sinoaortic baroreceptor denervation and sinoaortic baroreceptor plus vagal denervation, mean arterial pressure remained at its control level only through 8 +/- 1 and 4 +/- 1 ml/kg hemorrhage, respectively. The increases in renal nerve activity during nonhypotensive hemorrhage were significantly attenuated by either sinoaortic baroreceptor or cardiac denervation, and were completely blocked by sinoaortic baroreceptor plus vagal denervation. However, the decline in renal nerve activity with hypotensive hemorrhage was not blocked by either cardiac or sinoaortic baroreceptor denervation, and was enhanced after sinoaortic baroreceptor plus vagal denervation. Our data indicate that nonhypotensive hemorrhage in the conscious dog elicits a striking increase in renal nerve activity, which then returns to control levels during hypotensive hemorrhage. Both sinoaortic and cardiopulmonary baroreceptors are involved in mediating the increase in renal nerve activity, whereas the decline in renal nerve activity is not due to either of these baroreflexes.