ANGIOTENSIN-II - A HUMORAL MEDIATOR FOR THE GASTRIC SODIUM MONITOR

Natriuresis in direct response to a gastric sodium stimulus (upper-gut sodium monitor) has paradoxically only been demonstrated in humans an d animals on a low-sodium diet preceding each study. It is possible th at the low-sodium diet itself induces or suppresses systems that media te or oppose the ensuing natriuresis. In this study, we sought to dete rmine whether a system activated by this diet, the renin-angiotensin s ystem, mediates the natriuretic response. Specifically, we sought to s how whether changes in the circulating concentration of angiotensin II (ANG II) may mediate the renal response to stimulation of the gastric sodium monitor. Male New Zealand White rabbits were randomly assigned to low- (0.008%) or normal (2.2%) sodium diets. After 1 wk on the exp erimental diet, they received a sodium load intragastrically or intrav enously, and plasma ANG II was measured at 0, 5, 10, 30, 60, and 120 m in. Urine was collected for 4 h after the sodium load, and plasma sodi um was measured at 0, 2, and 4 h. Urinary sodium excretion was greater in the 4 h after gastric than after intravenous sodium administration (P < 0.025) in the rabbits on the low-sodium diet. No significant dif ference was noted in the rabbits on the normal sodium. In rabbits on t he low-sodium diet, there was an immediate and significant decline in plasma ANG II after sodium was administered both intragastrically (P < 0.025) and intravenously (P < 0.05). This decrease was greater after intragastric than intravenous sodium (P < 0.0025), and the difference was still evident at 120 min (P < 0.05). No significant difference in plasma ANG II was found in the normal diet group. We conclude, therefo re, that a prolonged decrease in ANG II concentration may play a role in mediating the natriuretic response to the gastric sodium monitor.