Sodium ions absorbed from the intestine are postulated to act on the liver to reflexly suppress renal sympathetic nerve activity (RSNA), resulting in inhibition of sodium reabsorption in the kidney. To test the hypothesis that the renal sympathoinhibitory response to portal venous NaCl infusion involves an action of arginine vasopressin (AVP) at the area postrema, we examined the effects of portal venous infusion of hypertonic NaCl on RSNA before and after lesioning of the area postrema (APL) or after pretreatment with an AVP V1 receptor antagonist (AVPX). Rabbits were chronically instrumented with portal and femoral venous 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−1of 9.0% NaCl for 10 min) produced a dose-dependent suppression of RSNA (−12 ± 3, −34 ± 3, −62 ± 5, and 80 ± 2%, respectively) 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% NaCl 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 significant differences between the effects of AVPX and APL, and the effect of APL was not augmented by AVPX. These results indicate that the suppression of RSNA due to portal venous infusion of 9.0% NaCl involves an action of AVP via the area postrema.
High dietary sodium intake sensitizes the pressor and renal sympathetic nerve activity responses to peripheral and spinal vasopressin infusion