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1 I. Physiologisches Institut
der Ruprecht-Karls-Universität Heidelberg,
Exogenous endothelin-1 (ET-1) is a strong vasoconstrictor in the
canine kidney and causes a decrease in renal blood flow (RBF) by
stimulating the ETA receptor
subtype. The aim of the present study was to investigate the role of
endogenously generated ET-1 in renal hemodynamics under physiological
conditions. In six conscious foxhounds, the time course of the effects
of the selective ETA receptor
antagonist LU-135252 (10 mg/kg iv) on mean arterial blood pressure
(MAP), heart rate (HR), RBF, and glomerular filtration rate (GFR), as
well as its effects on renal autoregulation, were examined. LU-135252
increased RBF by 20% (from 270 ± 21 to 323 ± 41 ml/min, P < 0.05) and HR from
76 ± 5 to 97 ± 8 beats/min (P < 0.05), but did not alter MAP, GFR, or autoregulation of RBF and
GFR. Since a number of interactions between ET-1 and the
renin-angiotensin system have been reported previously, experiments
were repeated during angiotensin converting enzyme (ACE) inhibition by
trandolaprilat (2 mg/kg iv). When
ETA receptor blockade was combined
with ACE inhibition, which by itself had no effects on renal
hemodynamics, marked changes were observed: MAP decreased from 91 ± 4 to 80 ± 5 mmHg (P < 0.05), HR
increased from 85 ± 5 to 102 ± 11 beats/min (P < 0.05), and RBF increased from
278 ± 23 to 412 ± 45 ml/min (P < 0.05). Despite a pronounced decrease in renal vascular resistance over the entire pressure range investigated (40-100 mmHg), the capacity of the kidneys to autoregulate RBF was not impaired. The GFR
remained completely unaffected at all pressure levels. These results
demonstrate that endogenously generated ET-1 contributes significantly
to renal vascular tone but does not interfere with the mechanisms of
renal autoregulation. If ETA
receptors are blocked, then the vasoconstrictor effects of ET-1 in the
kidney are compensated for to a large extent by an augmented influence
of ANG II. Thus ET-1 and ANG II appear to constitute a major
interrelated vasoconstrictor system in the control of RBF.
ETA receptor blockade; renal hemodynamics; renal autoregulation; renin-angiotensin system
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