Parallel regulation of constitutive nitric oxide synthase and renin at the juxtaglomerular apparatus of rat kidney under various stimuli. Bosse, Hans Martin, Rita B[diaeresis]ohm, Stefan Resch, and Sebastian Bachmann. Department of Anatomy and Cell Biology I, University of Heidelberg, Heidelberg, Germany
APStracts 2:0093F, 1995.
Four chronic experiments were performed to assess changes in the activity and gene expression of type I nitric oxide synthase (NOS) at the macula densa (MD) and of renin expression and immunoreactivity (IR) at the juxtaglomerular apparatus (JGA) of rat kidney: (A) two -kidney, one-clip Goldblatt hypertension (2K1C, for 3 and 40 days, sham operation for controls), (B) furosemide treatment (150 mg/kg/d i.p. for 5 days), (C) chronic low salt diet (0.02%) vs. high salt diet (3%; both for 11 days), and (D) chronic blockade of NOS by nitro-L-arginine-methylester (L-NAME, 40mg/kg/d for 2 months). NOS and renin gene expression, NOS enzyme activity and renin IR were semiquantitatively evaluated with histochemical methods (NADPH diaphorase, in situ hybridization, immunohistochemistry). In 2K1C marked increases were induced in NOS and renin in the ischemic vs. contralateral kidneys both after 3 and 40 days, respectively (p&LT.05). Related to controls, significant increases in the ischemic kidney were encountered after 3 and 40 days, while contralateral suppression of NOS and renin was found only after 40 days. Furosemide treatment resulted in a marked increase of both NOS and renin levels when compared to controls (p&LT.05). Salt restriction induced a significant elevation of NOS levels when compared to salt loading (p&LT.05), while only minor changes were evident in renin levels. L-NAME treatment resulted in a moderate reduction of NOS activity (n.s.), while renin levels were markedly reduced (p&LT.05). These results show that NOS activity and gene expression are inversely related to chronic changes in renal perfusion, salt balance and salt transport at the distal tubule in parallel with the known response of renin to these changes. Inhibition of NOS decreases renin levels at the JGA. The histochemical findings support previous concepts that MD derived NO is involved in the control of renin synthesis. 

Received 24 February 1995; accepted in final form 1 June 1995.
APS Manuscript Number F66-5.
Article publication pending Am. J. Physiol. (Renal Fluid Electrolyte
Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on  6 July 1995.