Intrarenal Role of Angiotensin II
HOMEOSTATIC REGULATION OF RENAL BLOOD FLOW IN THE DOG
The analogue, l-sarcosine-8-alanine-angiotensin II, a specific competitive antagonist of the vascular action of angiotensin II in the rat, blocked the decrease in renal blood flow after a single intrarenal injection of angiotensin II but not after an injection of norepinephrine in normal dogs, in a sodium-depleted dog, and in a dog with thoracic vena caval constriction. Infusion of the analogue at 0.2 µg/kg min-1 into the renal artery consistently increased renal blood flow and decreased renal resistance in both sodium-depleted dogs and dogs with vena caval constriction but did not alter these functions in normal dogs. In five sodium-depleted dogs, renal blood flow increased from an average control value of 196 ± 5 ml/min to 222 ± 11 and 246 ± 12 ml/min after 20 and 40 minutes of antagonist infusion (P < 0.01 and P < 0.005, respectively); renal resistance fell from 0.71 ± 0.03 mm Hg/ml min-1 to 0.62 ± 0.06 and 0.54 ± 0.03 mm Hg/ml min-1 (P < 0.005 for the 40-minute value). In five dogs with vena caval constriction, renal blood flow increased from 143 ± 16 ml/min to 178 ± 23 and 190 ± 19 ml/min after 20 and 40 minutes of analogue infusion (P < 0.02 and P < 0.005, respectively); renal resistance fell from 0.90 ± 0.14 mm Hg/ml min-1 to 0.73 ± 0.14 and 0.64 ± 0.10 mm Hg/ml min-1 (P < 0.01 and P > 0.02, respectively). Mean arterial blood pressure was not altered significantly by the analogue when it was infused at 0.2 µg/kg min-1. Infusion of the analogue at 2.0µ/kg min-1 decreased arterial blood pressure and renal resistance and increased renal blood flow in five sodium-depleted dogs and in three dogs with vena caval constriction. These observations suggest an important intrarenal role for angiotensin II in the homeostatic regulation of renal blood flow in sodium-depleted dogs and in dogs with vena caval constriction.
- angiotensin II analogue
- angiotensin II antagonist
- renal resistance
- sodium depletion
- vena caval constriction
- Received January 12, 1973.
- Accepted March 29, 1973.
- © 1973 American Heart Association, Inc.