1: Hypertension. 1992 Apr;19(4):333-8. 

Pressure natriuresis in rats during blockade of the L-arginine/nitric oxide
pathway.

Johnson RA, Freeman RH.

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

The natriuretic response was studied in anesthetized rats during the intravenous
infusion of L-arginine analogues to inhibit the production of
endothelium-derived nitric oxide. In an initial experimental series, rats were
administered saline vehicle or vehicle containing 300 mumol/kg body wt N
omega-monomethyl-L-arginine, N omega-nitro-L-arginine methyl ester, N
omega-monomethyl-D-arginine, or L-arginine. Infusion of the competitive
inhibitors N omega-monomethyl-L-arginine and N omega-nitro-L-arginine methyl
ester significantly increased mean arterial pressure to 155 +/- 3 and 145 +/- 5
mm Hg, respectively, compared with a mean arterial pressure of 118 +/- 3 mm Hg
determined in the vehicle control group. Sodium excretion averaged 3.27 +/- 1.08
and 2.52 +/- 0.78 mu eq/min in the N omega-monomethyl-L-arginine- and N
omega-nitro-L-arginine methyl ester-treated rats, respectively, and each was
significantly higher than the basal sodium excretion of 0.20 +/- 0.05 mu eq/min
in the vehicle-treated control animals. Plasma renin activity was significantly
lower in the N omega-monomethyl-L-arginine- and N omega-nitro-L-arginine methyl
ester-treated groups than in the vehicle-treated group. Neither L-arginine nor N
omega-monomethyl-D-arginine administration significantly altered any of the
measured variables compared with vehicle alone. In a second experimental series,
an adjustable snare was placed around the suprarenal aorta for the purpose of
controlling renal perfusion pressure independently of increases in the systemic
mean arterial pressure initiated by infusion of N omega-nitro-L-arginine methyl
ester (75 mumol/kg i.v.).(ABSTRACT TRUNCATED AT 250 WORDS)

PMID: 1313394 [PubMed - indexed for MEDLINE]