Hypertension, Vol 22, 62-66, Copyright © 1993 by American Heart Association
AJ Stingo, AL Clavell, LL Aarhus and JC Burnett Jr
The current study was undertaken to define a biological role for the
endothelin-A receptor in a clinically relevant model of altered systemic
and renal function produced by suprarenal aortic cross- clamping. This
model is associated with profound systemic and renal vasoconstriction,
acute renal failure, and a significant increase in circulating endothelin.
Studies were performed in three groups of anesthetized mongrel dogs. Group
1 (n = 5) underwent aortic cross- clamping for 1 hour; group 2 (n = 5)
underwent aortic cross-clamping for 1 hour in the presence of BQ-123, a
specific antagonist of the endothelin-A receptor; group 3 (n = 4) received
BQ-123 alone. The marked systemic and renal vasoconstriction associated
with aortic cross- clamping in group 1 was markedly attenuated in group 2
in the presence of BQ-123. Unlike the vasoconstrictor response, BQ-123 did
not attenuate the decrease in glomerular filtration rate associated with
this model. Under unstimulated conditions in group 3, BQ-123 had no actions
on systemic or renal hemodynamics. In conclusion, the current study
demonstrates that the systemic and renal vasoconstriction associated with
aortic cross-clamping are in part mediated through the interaction of
endothelin and the endothelin-A receptor. This study demonstrates the
functional importance of increased endogenous endothelin in the regulation
of vascular tone in this pathophysiological state.
ARTICLES
Biological role for the endothelin-A receptor in aortic cross-clamping
Cardiorenal Research Laboratory, Mayo Clinic and Foundation, Rochester, MN 55905.
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