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Am J Physiol Regul Integr Comp Physiol 279: R2297-R2303, 2000;
0363-6119/00 $5.00
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Vol. 279, Issue 6, R2297-R2303, December 2000

Mechanisms of salt-sensitive hypertension: role of inducible nitric oxide synthase

Dunyong Y. Tan, Shumei Meng, Garrick W. Cason, and R. Davis Manning Jr.

Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi 39216

The goal of this study was to determine the role of inducible nitric oxide synthase (iNOS) in the arterial pressure, renal hemodynamic, renal excretory, and hormonal changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive (S) rats during changes in Na intake. Thirty-two R and S rats, equipped with indwelling arterial and venous catheters, were subjected to low (0.87 mmol/day) or high (20.6 mmol/day) Na intake, and selective iNOS inhibition was achieved with intravenous aminoguanidine (AG, 12.3 mg · kg-1 · h-1). After 5 days of AG, mean arterial pressure increased to 121 ± 3% control in the R-high Na AG rats compared with 98 ± 1% control (P < 0.05) in the R-high Na alone rats, and S-high Na rats increased their arterial pressure to 123 ± 3% control compared with 110 ± 2% control (P < 0.05) in S-high Na alone rats. AG caused no significant changes in renal hemodynamics, urinary Na or H2O excretion, plasma renin activity, or cerebellar Ca-dependent NOS activity. The data suggest that nitric oxide produced by iNOS normally helps to prevent salt-sensitive hypertension in the Dahl R rat and decreases salt sensitivity in the Dahl S rat.

mean arterial pressure; nitric oxide; glomerular filtration rate; renal hemodynamics; urinary Na excretion; plasma renin activity


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