Why the study?
Does chronic nitric oxide blockade induce salt-sensitive hypertension and alter renal hemodynamics in conscious rats on a high salt diet?
Does chronic nitric oxide blockade induce salt-sensitive hypertension and alter renal hemodynamics in conscious rats on a high salt diet?
Nitric oxide is essential for maintaining renal medullary blood flow during high salt intake, preventing the development of salt-sensitive hypertension.
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Impaired medullary flow may promote salt sensitivity during nitric oxide blockade; leaves open translation to human hypertension.
This study examined the effects of alterations in salt-intake on blood pressure (BP) in rats chronically treated intravenously with or without the nitric oxide synthase (NOS) inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) (8.6 mg/kg/day). The changes in mean arterial pressure (MAP), the renal cortical and medullary blood flow (CBF and MBF), and the sodium balance were determined by implanted optical fibers and laser-Doppler flow measurement techniques in the conscious rats. The results showed that high salt intake (7.4 mEq/day) elevates CBF (139% +/- 15%), but has no significant effect on MAP or MBF in control rats; in L-NAME-treated rats, high salt intake elevates MAP, produces no change in CBF, and decreases MBF (51% +/- 14%), as well as increasing the sodium balance (0.26 +/- 0.23 mEq/day to 1.29 +/- 0.47 mEq/day). The present experiments indicated that NO appears to maintain the MBF during high salt intake and to prevent the changes in MAP, and, in the absence of NO, salt-sensitive hypertension develops. Nitric oxide plays an important role in the development of salt-sensitive hypertension with the change of MBF.
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Nakanishi et al. (2002) studied this question.
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