有哪些信誉好的足球投注网站activation of thiazide-sensitive co-transport by angiotensin ii in the cyp1a1-ren2 hypertensive rat血管紧张素ⅱ的激活thiazide-sensitive co-transport cyp1a1-ren2高血压老鼠.pdfVIP
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activation of thiazide-sensitive co-transport by angiotensin ii in the cyp1a1-ren2 hypertensive rat血管紧张素ⅱ的激活thiazide-sensitive co-transport cyp1a1-ren2高血压老鼠
Activation of Thiazide-Sensitive Co-Transport by
Angiotensin II in the cyp1a1-Ren2 Hypertensive Rat
1 1 1 3 1
Ali Ashek , Robert I. Menzies , Linda J. Mullins , Christopher O. C. Bellamy , Anthony J. Harmar ,
1 2 1 1
Christopher J. Kenyon , Peter W. Flatman , John J. Mullins , Matthew A. Bailey *
1 University/British Heart Foundation Centre for Cardiovascular Science, The University of Edinburgh, Edinburgh, United Kingdom, 2 Centre for Integrative Physiology, The
University of Edinburgh, Edinburgh, United Kingdom, 3 Department of Pathology, Edinburgh New Royal Infirmary, Edinburgh, United Kingdom
Abstract
Transgenic rats with inducible expression of the mouse Ren2 gene were used to elucidate mechanisms leading to the
development of hypertension and renal injury. Ren2 transgene activation was induced by administration of a naturally
occurring aryl hydrocarbon, indole-3-carbinol (100 mg/kg/day by gastric gavage). Blood pressure and renal parameters
were recorded in both conscious and anesthetized (butabarbital sodium; 120 mg/kg IP) rats at selected time-points during
the development of hypertension. Hypertension was evident by the second day of treatment, being preceded by reduced
renal sodium excretion due to activation of the thiazide-sensitive sodium-chloride co-transporter. Renal injury was evident
after the first day of transgene induction, being initially limited to the pre-glomerular vasculature. Mircoalbuminuria and
tubuloinsterstitial injury developed once hypertension was established. Chronic treatment with either hydrochlorothiazide
or an AT1 receptor antagonist normaliz
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