CONTRIBUTION OF BARORECEPTORS TO THE CONTROL OF RENAL FUNCTION.

Abstract

Electrical stimulation of the left stellate ganglion of the dog is associated with an increase in urine flow, in electrolyte and total solute excretion, and in the renal clearance of inulin. These changes appear rapidly, are well maintained during prolonged stimulation, and stop soon after stimulation has ceased. The hemodynamic responses associated with these changes are an increase in arterial pulse pressure, an increase or no change in mean arterial blood pressure, and a decline in mean left atrial pressure. The diuretic response to stellate ganglion stimulation is diminished, but not abolished, by bilateral cervical vagotomy as are the changes in electrolyte excretion, total solute excretion, and the renal clearance of inulin. However, the hemodynamic responses are not greatly modified by cervical vagotomy. Vagotomy just above the diaphragm does not appear to modify these responses. The effect of vagotomy on the renal responses to stellate stimulation appears to be a result of sectioning baroreceptor afferent nerves which traverse the vagus nerves. The rapidity of the renal response to stellate stimulation, its temporal relation to the hemodynamic changes, and the effect of cervical vagotomy indicate that the diuresis is, to a large degree, secondary to withdrawal of renal sympathetic vasoconstrictor nerve discharge. The similarities between the renal responses to stellate stimulation and to intravenous infusions indicate that infusion diuresis may be mediated, at least in part, by the same mechanism. When renal blood flow is measured directly in the perfused kidney, carotid occlusion is associated with little change or with a decrease in renal blood flow at a time when renal arterial pressure increases. When renal blood flow is maintained constant in the perfused kidney, carotid artery occlusion is associated with an increase in renal arterial pressure. The intrarenal administration of the adrenergic blocking agent, phenoxybenzamine, can prevent the increase in renal vascular resistance during carotid occlusion indicating that it is due to an adrenergic mechanism. The renal pressure-flow curve is displaced down and to the right during carotid occlusion; autoregulation of renal blood flow is still observed, although at a lower level of blood flow. All these changes indicate that the primary renal response to carotid occlusion is vasoconstriction mediated by the renal sympathetic nerves. It is well-known that urine flow increases when renal arterial pressure is increased independent of a change in the activity of the renal vasoconstrictor nerves and independent of a change in renal blood flow. Consequently, the rise in arterial pressure associated with carotid occlusion can contribute directly to the response of the kidney to carotid occlusion. The variability of the changes in water and electrolyte excretion by the kidney during carotid occlusion may represent a varying contribution of direct and reflex mechanisms to the total response.