Interactions between XXXX and angiotensin II in controlling glomerular filtration.

@entity8 @entity859 @entity7308 @entity235 @entity177 @entity1122
This study examined interactions between @entity859 ( @entity7308 ) and angiotensin II (ANG II) in controlling @entity8 ( @entity8 ) and glomerular filtration rate (GFR). In six normal @entity235 , intrarenal @entity7308 infusion (1.0 mumol/min) transiently decreased @entity8 , but during sustained @entity7308 infusion @entity8 increased to 122 +/- 7% of control, although GFR remained at 75 +/- 6% of control. Blockade of ANG II formation with the converting enzyme inhibitor SQ 14225 (n = 6) almost abolished the transient decrease in @entity8 but did not prevent the sustained fall in GFR caused by @entity7308 . When circulating ANG II was held constant by intravenous infusion of SQ 14225 and 20 ng . kg-1 . min-1 of ANG II (n = 6), @entity7308 transiently decreased @entity8 but the return of @entity8 was much slower than in normal @entity235 and @entity8 did not increase above control. Maintenance of constant circulating ANG II did not prevent @entity7308 -mediated decreases in GFR. These observations suggest that @entity7308 -mediated reductions in GFR do not depend entirely on ANG II and may be due to dilation of efferent arterioles by @entity7308 . However, the transient renal vasoconstriction caused by @entity7308 depends on ANG II, and data from this study suggest that part of the waning constrictor response to @entity7308 is due to suppression of @entity1122 secretion and endogenous ANG II formation. In circumstances where high ANG II levels are maintained (i.e., @entity177 ), @entity7308 may be capable of causing sustained renal vasoconstriction.
