Effects of hemorrhage on renal nerve activity in conscious dogs.

Abstract

SUMMARY. 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 eitheT sinoaron'c 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. {CircRes 57: 788-793, 1985)

Negative feedforward control of body fluid homeostasis by hepatorenal reflex

“…62 Therefore, it is possible that the cardiopulmonary volume receptor is unloaded, and the renal sympathetic nerve is then reflexively activated. 63 Consistent with this, an increase in the central blood volume with no effect on the total blood volume, induced by head-out water immersion, which is known to reduce renal sympathetic nerve activity via the cardiopulmonary volume receptor, 64,65 significantly improves the renal excretory function. 66 Increased hepatic portal pressure is the other factor responsible for the increased renal sympathetic nerve activity.…”

Normovolaemia defined by central blood volume and venous oxygen saturation

“…in the apex of the heart) meet at the end of systole. The reflex may also originate in receptors within the pulmonary vessels 71 or the central veins. 72 These possibilities are not mutually exclusive and each may contribute to generate a vasovagal syncope leaving its specific origin unknown.…”

Yohimbine in neurally mediated syncope. Pathophysiological implications.

“…Experiments in animals have demonstrated that despite bilateral vagotomy or total cardiac denervation, sympathetic nerve activity falls (in a manner reminiscent of neurally mediated syncope) during hypotensive hemorrhage (11). In humans, neurally mediated hypotension and bradycardia with preceding sympathetic withdrawal have been similarly observed in patients with intact and with denervated ventricles (i.e., heart transplant patients) (12,13).…”