Stimulation of renin secretion by no-donors is related to the
cyclic-amp pathway.
Kurtz, Armin, Karl-Heinz G[diaeresis]otz, Marlies Hamann, Martin
Kieninger, Charlotte Wagner.
Institut f[umlaut]ur Physiologie der Universit[umlaut]at
Regensburg, Germany
APStracts 5:0014F, 1998.
This study aimed to characterize the cellular pathways along which
nitric oxide influences the secretion of renin from the kidney. Using
the isolated perfused rat kidney model we found that the NO-donor
sodium-nitroprusside (SNP) (1-30 (mol/l) induced a prompt
concentration dependent 4-fold increase of basal renin secretion. The
membrane permeable cGMP analogues 8-bromo-cGMP and 8-pCPT cGMP (5
-50(mol/l) inhibited basal renin secretion and attenuated the
stimulation of renin secretion by SNP. Conversely, the renin
stimulatory effect of SNP was enhanced in the presence of the G
-kinase inhibitor Rp-8CPTcGMPS (10(mol/l) The renin stimulatory effect
of SNP was amplified in nominally calcium free perfusate and was
abolished in the presence of angiotensin II (1nmol/l). Renin
secretion stimulated by SNP was clearly attenuated by the A-kinase
inhibitor Rp-8CPTcAMPS (25(mol/l).
These findings indicate that the renin stimulatory effect of NO-donors
in renal juxtaglomerular cells cannot be explained by activation of
G-kinase and is also less likely to be causally related to the
regulation of renin secretion by calcium. Since A-kinase activity is
required for the stimulation of renin secretion by SNP it appears as
if the renin stimulatory effect is causally related to the cAMP
pathway controlling renin secretion.
Received 7 May 1997; accepted in final form 5 January 1998.
APS Manuscript Number F154-7.
Article publication pending Am. J. Physiol. (Renal Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 28 January 1998