SUPPRESSION OF RENAL SYMPATHETIC-NERVE ACTIVITY DURING PORTAL-VEIN INFUSION OF HYPERTONIC SALINE

Sodium ions absorbed from the intestine are postulated to act on the l iver to reflexly suppress renal sympathetic nerve activity (RSNA), res ulting in inhibition of sodium reabsorption in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venou s NaCl infusion involves an action of arginine vasopressin (AVP) at th e area postrema, we examined the effects of portal venous infusion of hypertonic NaCl on RSNA before and after lesioning of the area postrem a (APL) or after pretreatment with an AVP V-1 receptor antagonist (AVP X). Rabbits were chronically instrumented with portal and femoral veno us catheters, femoral arterial catheters, and renal nerve electrodes. Portal venous infusion of 9.0% NaCl (0.02, 0.05, 0.10, and 0.15 ml.kg( -1).min(-1) of 9.0% NaCl for 10 min) produced a dose-dependent suppres sion of RSNA (-12 +/- 3, -34 +/- 3, -62 +/- 5, and 80 +/- 2%, respecti vely) that was greater than that produced by femoral vein infusion of 9.0% NaCl (2 +/- 3, -3 +/- 2, -12 +/- 4, and -33 +/- 3%, respectively) . The suppression of RSNA produced by portal vein infusion of 9.0% NaC l was partially reversed by pretreatment with AVPX (-9 +/- 3, -20 +/- 3, -41 +/- 4, and -55 +/- 4%, respectively) and by APL (-11 +/- 2, -25 +/- 2, -49 +/- 3, and -59 +/- 6%, respectively). There were no signif icant differences between the effects of AVPX and APL, and the effect of APL was not augmented by AVPX. These results indicate that the supp ression of RSNA due to portal venous infusion of 9.0% NaCl involves an action of AVP via the area postrema.