Hypertension, Vol 7, 32-38, Copyright © 1985 by American Heart Association
M Maier, M Starlinger, Z Zhegu, H Rana and BR Binder
Aprotinin, the serine protease inhibitor that also inhibits glandular
(urinary) kallikrein, or vehicle was infused into the aorta above the renal
arteries of anesthetized pigs. Renal hemodynamic and functional parameters
were followed over time and during hemorrhagic hypotension. Both renal
cortical blood flow and glomerular filtration rate were maintained in
vehicle-treated animals at mean arterial pressures as low as 70 mm Hg. As
long as renal cortical blood flow and glomerular filtration rate were
maintained during the progressive hypotension, urinary excretion rate of
kallikrein (as defined by kinin-generating activity) was increased. In
contrast, all aprotinin-treated animals had a decreased excretion rate, and
the renal cortical blood flow declined with the mean arterial pressure
during hemorrhage. The pattern of glomerular filtration rate and plasma
renin activity was comparable in both aprotinin-treated and vehicle-treated
hemorrhaged animals. Our findings suggest that the endogenous renal
kallikrein-kinin system is required for functional renal vasodilatation to
maintain renal cortical blood flow during hemorrhage and is therefore
directly or indirectly responsible for adjustment of preglomerular
resistance.
ARTICLES
Effect of the protease inhibitor aprotinin on renal hemodynamics in the pig
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