Effects of altered NaCl intake on renal hemodynamic and renin release responses to RNS

Relationships between frequency of renal nerve stimulation (RNS) and renal blood flow (RBF), glomerular filtration rate (GFR), and plasma renin activities (PRA) were evaluated in anesthetized dogs placed on low (5 meq/day)-, normal (40 meq/day)-, and high (200 meq/day)-sodium chloride diets. Arterial pressure, RBF, GFR, and renal venous and arterial PRA were determined before and during direct electrical RNS at 0.5, 1.0, and 2.0 Hz (15 V, 1.0 ms). Dogs on low sodium intakes increased renal venous PRA at 0.5-, 1.0-, and 2.0-Hz RNS, whereas dogs on normal sodium intakes did not increase renal venous PRA until RNS reached 2.0 Hz. High sodium dogs did not increase PRA at any frequency of RNS tested. RNS at 0.5 Hz was not associated with any changes in GFR or RBF in any of the groups. Dogs on normal sodium and high sodium intakes decreased both GFR and RBF during 1.0- and 2.0-Hz RNS. Low-sodium dogs, however, only decreased GFR and RBF during 2.0-Hz RNS, and these hemodynamic responses were significantly <2.0-Hz GFR and RBF responses of high sodium dogs. These data indicate that renal vasoconstrictor responses to RNS are potentiated, and renin release responses to RNS are potentiated, and renin release responses to RNS are reduced by elevation of sodium chloride intake. We suggest that during low sodium intake, activation of sympathetic nerve activity elicits an enhanced renin release response, whereas the renal vasculature may be protected against neurogenic vasoconstriction.