1: Am J Physiol. 1994 Jun;266(6 Pt 2):R1723-9. 

Renin release in rats during blockade of nitric oxide synthesis.

Johnson RA, Freeman RH.

Department of Physiology, University of Missouri School of Medicine, Columbia
65212.

The influence of renal perfusion pressure on renin release was examined in rats
administered the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl
ester (L-NAME). Compared with the control plasma renin of 6.0 +/- 0.7 ng
angiotensin I (ANG I).ml-1.h-1, plasma renin activity was suppressed (1.8 +/-
0.2 ng ANG I.ml-1.h-1, P < 0.05) in L-NAME-treated animals in which the renal
perfusion pressure was permitted to increase and reached 141 +/- 8 mmHg. Plasma
renin activity also was suppressed (2.5 +/- 0.4 ng ANG I.ml-1.h-1, P < 0.05) in
a second L-NAME-treated group in which the renal perfusion pressure was
controlled to a level of 105 +/- 5 mmHg via tightening of a suprarenal aortic
snare. Plasma renin activity was increased (12.0 +/- 1.4 ng ANG I.ml-1.h-1, P <
0.05) in a third L-NAME-treated group in which renal perfusion pressure was
reduced to 59 +/- 1 mmHg. Overall, these findings suggest that the intrarenal
pressure-sensing mechanism for renin release does not stringently require nitric
oxide synthesis. In a second experimental series, bilaterally renal-denervated
rats were administered L-NAME, and again plasma renin activity was suppressed
significantly whether renal perfusion pressure was permitted to increase or was
controlled. Thus L-NAME also suppressed plasma renin activity independently of
reflex reductions in renal neuroadrenergic activity even when renal perfusion
pressure was controlled. Infusions of sodium nitroprusside completely inhibited
L-NAME-induced suppression of plasma renin activity in these renal-denervated
rats. Nitric oxide may function as a paracrine stimulatory mechanism for the
local regulation of renin release.

PMID: 8024020 [PubMed - indexed for MEDLINE]