Control of glomerular filtration rate: role of intrarenally formed angiotensin II

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Abstract
The role of intrarenally formed angiotensin II (ANG II) in controlling glomerular filtration rate (GFR) during reduction of renal artery pressure (RAP) was studied. The experimental design prevented renin released by the kidney from entering the systemic circulation and therefore prevented changes in circulating ANG II from influencing GFR control. In dogs with only a functional intrarenal renin-angiotensin system (RAS), GFR and renal blood flow (RBF) were not significantly altered by RAP reduction to 70 mmHg. After blockade of intrarenal ANG II formation with SQ 14225 [3-mercapto-2D-methylpropanoyl-L-proline], reduction of RAP to 70 mmHg decreased GFR and filtration fraction to 75.6 7U 7.0 and 59.0 .+-. 4.1% of control, respectively, while RBF remained at 129.3 .+-. 8.8% of control. Calculated efferent arteriolar resistance decreased considerably more when RAP was reduced after SQ 14225, whereas preglomerular resistance decreased to about the same level as observed prior to SQ 14225 infusion. After return of endogenously produced ANG II by recirculation of the renal venous blood or after infusion of ANG II (following SQ 14225) at a rate that restored RBF to the control level (with RAP held at 70 mmHg in each case), GFR, filtration fraction and calculated efferent resistance were restored to control levels, but preglomerular resistance did not change. Intrarenal ANG II formation evidently plays an important role in maintaining GFR during reductions in RAP by constricting efferent arterioles. Increased circulating ANG II also appears to be important in preventing reductions in efferent arteriolar resistance and GFR following RAP reduction.