Gastric acid secretion after blockade of angiotensin AT1 receptors in the Na(+)-depleted rat.

This study tested the hypothesis that angiotensin II acting through the angiotensin AT1 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 microgram/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 AT1 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 AT1 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 suggested that the decrease in pentagastrin-stimulated acid secretion in Na(+)-depleted animals is mediated by angiotensin II acting through the angiotensin AT1 receptor, most probably through vascular mechanisms.