(Hypertension. 1997;30:409.)
© 1997 American Heart Association, Inc.
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From the Franz Volhard Clinic and the Max Delbrück Center for Molecular Medicine (A.L., V.G., K.S., W.S., M.B., F.C.L.), Virchow Klinikum, Humboldt University, Berlin, Germany; Department of Neuroscience, Division of Cellular and Molecular Neurochemistry, Karolinska Institute (A.H.), Stockholm, Sweden; INSERM U358 (S.N.), Paris, France; and Barzilai Medical Center (C.Y., Y.Y.), Ashkelon, Ben Gurion University, Israel.
Correspondence to Friedrich C. Luft, Franz Volhard Clinic, Wiltbergstr 50, 13122 Berlin, Germany. E-mail fcluft{at}mdc-berlin.de
Abstract The molecular mechanisms of salt sensitivity and the contribution of the kidney to salt-induced hypertension in Sabra rats are imperfectly defined. We investigated the expression of the nitric oxide (NO) system (endothelial, inducible, and neural NO synthases) and renin-angiotensin system (renin, angiotensinogen, and angiotensin II type 1A receptor) gene components in the kidneys of SBN/y (salt-resistant) and SBH/y (salt-sensitive) Sabra rat substrains, with and without deoxycorticosterone acetate (DOCA)salt treatment. We also looked for immunocytochemical evidence of angiotensin II, the effector peptide of the renin-angiotensin system. Inducible and neural NO synthase gene expression values were lower in SBH/y than in SBN/y before and after DOCA-salt treatment. The gene expression level of endothelial NO synthase was not different in SBH/y and SBN/y, either with or without DOCA salt. Renin gene expression was significantly higher in kidneys of SBN/y than in kidneys of SBH/y rats, whereas angiotensinogen gene expression was significantly lower in SBN/y. After DOCA-salt treatment, renin gene expression was strongly suppressed in both strains but more so in SBH/y. Angiotensinogen gene expression, on the other hand, was increased by DOCA salt in SBN/y rats so that the two strains were no longer different. Angiotensin II immunoreactivity was significantly higher in SBN/y than in SBH/y; however, after DOCA salt, immunoreactivity in both strains was no longer detectable. Angiotensin II type 1A receptor gene expression was not different between the two strains, either before or after DOCA-salt administration. We conclude that DOCA salt induced a decrease in the activity of the renin-angiotensin system but did not change NO synthase gene expression in SBH/y and SBN/y. Inducible and neural NO synthase gene expression values were less in SBH/y than in SBN/y, independent of DOCA-salt administration. Thus, the NO system could explain, at least in part, the salt resistance of SBN/y.
Key Words: hypertension, renal salt gene expression renin-angiotensin system nitric oxide
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