Gastric acid secretion after blockade of angiotensin AT 1 receptors in the Na +-depleted rat

Abstract

This study tested the hypothesis that angiotensin II acting through the angiotensin AT 1 receptor plays an important role in the control of gastric acid secretion. Basal gastric acid secretion and gastric blood flow were lower in Na +-depleted animals, in which the renin-angiotensin system was activated, than in animals maintained on a normal Na + diet. Intravenous infusion of pentagastrin at 0.6 μg/kg/min increased gastric acid secretion to a greater extent in normal Na + than in Na +-depleted animals. In addition to stimulating gastric acid secretion, pentagastrin increased gastric blood flow by proportionally the same amount in both normal and low Na + animals. However, because basal gastric blood flow was considerably reduced in Na +-depleted animals, the increase produced by pentagastrin extended only to the levels observed in non-pentagastrin-treated normal Na + animals. Lower gastric blood flow in response to pentagastrin may explain the smaller increase in gastric acid secretion observed in Na +-depleted animals. In Na +-depleted animals, the selective angiotensin AT 1 receptor antagonist losartan did not affect basal gastric acid secretion or gastric blood flow, suggesting the involvement of mechanisms other than angiotensin II. Following blockade of angiotensin AT 1 receptors, pentagastrin significantly increased gastric blood flow in Na +-depleted animals to levels observed with infusion of the pentapeptide in normal Na + animals. The results suggest that the decrease in pentagastrin-stimulated acid secretion in Na +-depleted animals is mediated by angiotensin II acting through the angiotensin AT 1 receptor, most probably through vascular mechanisms.