AJP - Regulatory, Integrative and Comparative Physiology, Vol 245, Issue 2 166-R173, Copyright © 1983 by American Physiological Society
Renal hemodynamic actions of angiotensin II: interaction with tubuloglomerular feedback
J. E. Hall and J. P. Granger
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.
