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The present study was designed to investigate the importance of interactions between angiotensin II (ANG II) and other intrinsic control mechanisms, including tubuloglomerular feedback (TGF), in controlling renal hemodynamics. When endogenous ANG II formation was blocked by SQ 14225 infusion and changes in myogenic activity were minimized by servo controlling renal arterial pressure, ANG II infusion (20 ng . kg-1 . min-1 iv) did not change glomerular filtration rate but decreased renal blood flow (RBF) from 286 +/- 36 to 179 +/- 31 ml/min due to increases in calculated preglomerular (54%) and efferent (100%) arteriolar resistances. After inhibition of TGF by occluding the ureter during mannitol diuresis, ANG II infusion (20 ng . kg-1 . min-1) decreased RBF from 229 +/- 25 to 151 +/- 19 ml/min while increasing glomerular hydrostatic pressure (calculated from ureteral stop-flow pressure and plasma colloid osmotic pressure) from 56.7 +/- 2.5 to 62.3 +/- 2.2 mmHg. Postglomerular resistance increased to 173 +/- 17% of control, but preglomerular resistance did not change significantly during ANG II infusion after inhibition of TGF. These data suggest that the direct renal vasoconstrictor action of ANG II is confined mainly to postglomerular vessels and that changes in preglomerular resistance that occur when ANG II levels are inappropriately elevated in normal animals are caused by other intrinsic control mechanisms, such as TGF.
Hall et al. (Mon,) studied this question.
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