Decreased renin release and constant kallikrein secretion after injection of L-NAME in isolated perfused rat kidney.
A possible role of the endothelial L-arginine/NO pathway in the control of renal hemodynamics, renin release and kallikrein secretion was studied in an isolated rat kidney model perfused in a closed-circuit. NG-nitro-L-arginine methyl ester (L-NAME, 1-50 microM), an inhibitor of nitric oxide biosynthesis, caused a dose-dependent increase in perfusion pressure (PP) and a dose-dependent decrease in renal perfusate flow. Renin release was inhibited independently of a rise in PP. L-NAME did not change the urinary kallikrein secretion. These results confirm the intervention of the L-arginine/NO pathway in the vasodilation of this isolated perfused kidney model and demonstrate the inhibitory effect of L-NAME on renin release. They suggest that nitric oxide synthesis plays a role in stimulating renin release and is not involved in the regulation of urinary kallikrein secretion.
Gardes
J
J
INSERM U36, Paris, France.
Poux
J M
JM
Gonzalez
M F
MF
Alhenc-Gelas
F
F
Menard
J
J
D000704:Analysis of Variance; D000818:Animals; D001120:Arginine / Q000031:analogs & derivatives* / Q000494:pharmacology; D066298:In Vitro Techniques; D007610:Kallikreins / Q000378:metabolism* / Q000652:urine; D007668:Kidney / Q000187:drug effects / Q000201:enzymology*; D007700:Kinetics; D019331:NG-Nitroarginine Methyl Ester; D010477:Perfusion; D051381:Rats; D012083:Renin / Q000378:metabolism*; D013997:Time Factors
D001120:Arginine; D007610:Kallikreins; D012083:Renin; D019331:NG-Nitroarginine Methyl Ester