STIMULATION OF GASTRIC OSMORECEPTORS BUT NOT THE SODIUM MONITOR INCREASES RENAL ANGIOTENSIN-CONVERTING ENZYME-ACTIVITY

1. Stimulation of the gastric sodium monitor has been reported to caus e a decrease in renal nerve activity and also a decrease in plasma ren in activity in renal venous blood. This suggests that changes in sympa thetic nerve activity and in the intrarenal renin-angiotensin system m ay mediate the natriuresis that occurs following gastric sodium admini stration, In the present study we sought to determine whether gastric sodium administration also modulates angiotensin-converting enzyme (AC E) activity in the kidney. 2. Male Sprague-Dawley rats were equilibrat ed on a low-sodium (0.008%) diet for 7 days. On the day of the experim ent, rats were anaesthetized and kidneys were harvested and immediatel y snap frozen at 0 and 60 min after intragastric administration of a s aline load (1.5 mmol/kg as 3 mol/L saline) or an equivalent volume of iso-osmotic urea (5.95%). Angiotensin-converting enzyme activity was d etermined by incubation of kidney homogenates with hippuryl-histidyl-l eucine and fluorometric assay of the histidyl-leucine generated. 3. An giotensin-converting enzyme activity in the kidney increased in respon se to the intragastric administration of both sodium chloride and urea . Angiotensin-converting enzyme activity increased significantly from control levels (189.9 +/- 24.3 nmol/min per g protein) by 60 min in bo th NaCl- and urea-treated groups (492.3 +/- 27.3 and 468.6 +/- 28.7 nm ol/min per g protein, respectively; P < 0.0005). 4. We conclude that i nstillation of sodium chloride or isoosmotic urea into the stomach inc reases ACE activity in the kidney, The results of the present study su ggest that this effect is due to changes in osmolality rather than sti mulation of the gastric sodium monitor.