Angiotensin II, renal nerves, and prostaglandins in renal hemodynamics during hemorrhage

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Abstract
The importance of renal prostaglandins (PG), angiotensin II and renal nerves in control of renal hemodynamics was examined in anesthetized dogs during a 30% reduction in arterial blood pressure by hypotensive hemorrhage (HH). In the 1st group of 8 PG-intact (control) animals, HH caused a modest decrease in both glomerular filtration rate (GFR) (from 46 to 37 ml/min, P < 0.05) and renal blood flow (RBF) (from 254 to 192 ml/min, P < 0.01). In the 2nd group of 6 dogs pretreated with indomethacin (10 mg/kg), a striking fall in both GFR (from 47 to 5 ml/min, P < 0.001) and RBF (from 213 to 25 ml/min, P < 0.001) was observed with HH. Unilateral intrarenal infusion of a specific angiotensin II antagonist (AIIA) in these depleted animals significantly attenuated this ischemic effect of HH as both GFR (5 vs. 20 ml/min, P < 0.005) and RBF (25 vs. 87 ml/min, P < 0.01) were higher in the AIIA-infused kidneys. To assess the combined influence of both renal nerves and the renin-angiotensin system as renal ischemic factors during HH, a 3rd group of 8 indomethacin-treated dogs underwent unilateral renal denervation and infusion of the AIIA antagonist prior to HH. The denervated, AIIA-infused kidneys in these PG-depleted animals had significantly greater GRF (41 vs. 5 ml/min, P < 0.005) and RBF (183 vs. 29 ml/min, P < 0.005) than the contralateral innervated, uninfused kidneys. This combination of renal denervation and AIIA infusion afforded significantly greater protection of GRF (41 vs. 20 ml/min, P < 0.05) and RBF (183 vs. 87 ml/min, P < 0.05) during HH than AIIA alone in the PG-depleted animals. The renin-angiotensin system and renal nerves are major renal ischemic factors during HH of this degree, and these ischemic factors are normally opposed by renal PG.