RENAL INTERSTITIAL FLUID ANGIOTENSIN - MODULATION BY ANESTHESIA, EPINEPHRINE, SODIUM DEPLETION, AND RENIN INHIBITION

Using a microdialysis technique, we monitored changes in right and left renal interstitial fluid angiotensins in anesthetized and conscious dogs (both n=5) in response to right renal interstitial epinephrine (0.2 mg/kg per minute) administration. Renal interstitial and plasma angiotensin levels also were monitored in conscious dogs (n=4) in response to dietary sodium deprivation (10 mmol/d) for 5 consecutive days. Changes in renal interstitial and plasma angiotensins in response to interstitial administration of a specific renin inhibitor, ACRIP (0.5 mu g/kg per minute for 20 minutes), were monitored on day 5 of sodium depletion. At basal levels, there were no significant differences between the right and left renal interstitial immunoreactive angiotensin levels in anesthetized dogs. Renal interstitial epinephrine administration caused a significant increase in renal interstitial immunoreactive angiotensin concentrations in both anesthetized and conscious dogs (P<.01). However, anesthetized dogs had significantly higher renal interstitial immunoreactive angiotensin levels basally and in response to epinephrine than conscious dogs (P<.05). Renal interstitial immunoreactive angiotensin concentrations increased significantly and progressively during exposure to a low sodium diet from 3.9+/-1 nmol on day 1 to 740+/-332 nmol on day 5 (P<.01). Renal interstitial immunoreactive angiotensin decreased significantly to 124+/-37 nmol (P<.01) in response to intrarenal renin inhibition at the end of day 5 of sodium depletion. Plasma immunoreactive angiotensin increased significantly (P<.01) in response to sodium depletion, and no change occurred during intrarenal renin inhibition. We conclude that anesthesia, epinephrine, sodium depletion, and renin inhibition modulate renal interstitial angiotensin, which may serve as an important physiological regulator.