Adrenal, kidney, and heart angiotensins in female murine ren-2 transfected hypertensive rats

We analyzed by high-performance liquid chromatography and radioimmunoassay angiotensin I (Ang I), Ang II, Ang-(1–7), and metabolites in the adrenal, kidney and heart of normotensive female Sprague–Dawley (SD) and transgenic hypertensive [TGR(mRen-2)27] rats carrying the murine Ren-2 d renin gene. Th...

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Published inPeptides (New York, N.Y. : 1980) Vol. 19; no. 10; pp. 1685 - 1694
Main Authors Senanayake, P.deS, Smeby, R.R, Martins, A.S, Moriguchi, A, Kumagai, H, Ganten, D, Brosnihan, K.B
Format Journal Article
LanguageEnglish
Published United States Elsevier Inc 1998
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Summary:We analyzed by high-performance liquid chromatography and radioimmunoassay angiotensin I (Ang I), Ang II, Ang-(1–7), and metabolites in the adrenal, kidney and heart of normotensive female Sprague–Dawley (SD) and transgenic hypertensive [TGR(mRen-2)27] rats carrying the murine Ren-2 d renin gene. The monogenetic model of hypertensive rats had significant increases in adrenal Ang II; whereas in the kidney Ang II was unchanged, but Ang I and Ang-(1–7) were significantly lower. Cardiac Ang I, Ang II, and Ang-(2–10) were significantly reduced in transgenic rats, while Ang-(2–7) was increased. In SD and transgenic rats kidney and adrenal angiotensins increased primarily during estrus or proestrus. In female transgenic rats the increased adrenal Ang II and the sustained renal Ang II may contribute to the established phase of hypertension.
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ISSN:0196-9781
1873-5169
DOI:10.1016/S0196-9781(98)00123-5