TY - JOUR
T1 - Angiotensin II, renal nerves, and prostaglandins in renal hemodynamics during hemorrhage
AU - Henrich, W. L.
AU - Berl, T.
AU - McDonald, K. M.
PY - 1978
Y1 - 1978
N2 - 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 first group of eight 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 second group of six 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 third group of eight 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 GFR (41 vs. 5 ml/min, P < 0.005) and RBF (183 vs. 29 ml/min, P < 0.005) than the contralateral innervated, uninfused kidneys. Furthermore, this combination of renal denervation and AIIA infusion afforded significantly greater protection of GFR (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 results, therefore, indicate that 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.
AB - 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 first group of eight 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 second group of six 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 third group of eight 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 GFR (41 vs. 5 ml/min, P < 0.005) and RBF (183 vs. 29 ml/min, P < 0.005) than the contralateral innervated, uninfused kidneys. Furthermore, this combination of renal denervation and AIIA infusion afforded significantly greater protection of GFR (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 results, therefore, indicate that 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.
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U2 - 10.1152/ajprenal.1978.235.1.f46
DO - 10.1152/ajprenal.1978.235.1.f46
M3 - Article
C2 - 677317
AN - SCOPUS:0017986415
SN - 0363-6127
VL - 4
SP - F46-F51
JO - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
JF - American Journal of Physiology - Renal Fluid and Electrolyte Physiology
IS - 1
ER -