Sodium and vasopressin modulation of renal sympathetic nerve activity.
A series of correlative studies show that sympathetic renal nerve activity (RNA) may be influenced by the concentration of sodium (Na+) in the plasma and the cerebrospinal fluid (CSF). Further study of the sites and characteristics of the interaction between Na+ and the renal nerves was undertaken in anesthetized dogs. Cerebroventricular (i.c.v.) injections of hypertonic sodium chloride (NaCl) produced a sympathetic vasoconstrictor response associated with tachycardia, increases in plasma norepinephrine and vasopressin (AVP), and a decrease in the electroneurographic activity recorded from post-ganglionic renal sympathetic nerves. Both bilateral vagotomy and intravenous administration of an AVP antagonist prevented the decrease in RNA caused by i.c.v. hypertonic NaCl, without markedly reducing the magnitude of the pressor response. The same phenomenon, however, could not be duplicated by delivery of the AVP antagonist i.c.v. In another group of dogs, the pressor activity of NaCl injected into the cisterna magna was compared before and after surgical ablation of the area postrema in the dorsal medulla. Removal of this circumventricular organ attenuated the pressor effects of NaCl given into the cisterna magna, but not those produced by i.c.v. delivery of the injectate. The data suggest that acute increases in CSF Na+ cause a differential activation of the sympathetic nervous system mediated in part by structures at or near the area postrema. At this site, circulating AVP apparently augments the inhibitory input from vagal afferents on the preganglionic renal nerve neurons.