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Am J Physiol Regul Integr Comp Physiol (October 24, 2002). doi:10.1152/ajpregu.00509.2002
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Articles in PresS, published online ahead of print October 24, 2002
Am J Physiol Regu Physiol, 10.1152/ajpregu.00509.2002
Submitted on August 21, 2002
Accepted on October 22, 2002

Mechanisms of Salt-Sensitive Hypertension: Role of Renal Medullary Inducible Nitric Oxide Synthase

Niu Tian1, Anthony W Gannon1, Raouf A Khalil1, and R. Davis Manning, Jr.1*

1 Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA

* To whom correspondence should be addressed. E-mail: dmanning{at}physiology.umsmed.edu.

The goal of this study was to determine the role of renal medullary inducible nitric oxide synthase (iNOS) in the arterial pressure, renal hemodynamic and renal excretory changes that occur in Dahl/Rapp salt-resistant (R) and salt-sensitive (S) rats during high Na intake. Forty R and S rats, equipped with indwelling arterial, venous and renal medullary catheters were subjected to high (8%) Na intake, and selective iNOS inhibition was achieved with continuous IV or renal medullary interstitial infusion of aminoguanidine (AG, 3.075 mg/kg/h). After 5 days of AG, mean arterial pressure increased to 132 ± 2 % control in the S-high Na, AG-intramedullary rats compared to 121 ± 4 % control (P<0.05) in the S-high Na alone rats and 121 ± 2 % control (P<0.05) in the S-high Na, AG-IV rats. AG did not change arterial pressure in R rats. AG also caused little change in renal hemodynamics, urinary Na or H2O excretion or acetylcholine-induced aortic vasorelaxation in R or S rats. The data suggest that during high Na intake, nitric oxide produced by renal medullary iNOS helps to prevent excessive increases in arterial pressure in the Dahl S rat but not the R rat.




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