AJP - Heart and Circulatory Physiology, Vol 243, Issue 2 277-H283, Copyright © 1982 by American Physiological Society
No effect of intrarenal converting enzyme inhibition on canine renal blood flow
B. G. Zimmerman, P. C. Wong, G. K. Kounenis and E. J. Kraft
Captopril and teprotide were administered intra-arterially to the kidney
and intravenously to inhibit intrarenal and extrarenal converting enzyme
(CE), respectively. Captopril was infused at 0.4, 0.8, and 1.6 micrograms .
kg-1 . min-1 intra-arterially, and teprotide was given at 0.4 and 0.8
micrograms . kg-1 . min-1 intra-arterially in salt-replete dogs (group 1).
Both agents were also given intravenously in the dose of 0.2 mg/kg, known
to cause maximal extrarenal CE inhibition. The intra-arterial infusions of
the inhibitors had no effect on renal hemodynamics but caused a graded
degree of intrarenal CE inhibition. A lesser degree of extrarenal CE
inhibition was seen after captopril in these doses. Intravenous
administration of captopril and teprotide inhibited extrarenal CE, but only
captopril increased renal blood flow (13%). When teprotide was given in a
higher dose (group 3, 1.02 mg/kg), it too increased renal blood flow. In
salt-deplete dogs (group 2), captopril infused intra-arterially caused a
degree of intrarenal CE inhibition comparable with that in the salt-replete
dogs but again produced little or no renal hemodynamic changes. When given
intravenously in this group, captopril inhibited extrarenal EE and elicited
a greater increase in renal blood flow (36%) than in the group 1 dogs.
These results indicate that in conscious dogs renal vasodilatation is
associated with extrarenal, but not intrarenal, CE inhibition.
