Boecker, Wolfgang and Hupf, Harald and Grimm, Daniela and Kurzidim, Klaus and Schunkert, Heribert (2000) Effects of indapamide in rats with pressure overload left ventricular hypertrophy. JOURNAL OF CARDIOVASCULAR PHARMACOLOGY, 36 (4). pp. 481-486. ISSN 0160-2446
Full text not available from this repository. (Request a copy)Abstract
We studied the in vivo effects of the antihypertensive diuretic agent indapamide on left ventricular (LV) morphology in chronically pressure-overloaded rat hearts. LV pressure and subsequently LV mass were increased by banding the ascending aorta over a period of 6 weeks. Thereafter, animals were treated with low-dose (1 mg/kg/day, n = 9) or high-dose (10 mg/kg/day, n = 9) indapamide for another 6 weeks. Low-dose indapamide treatment reduced LV weights as compared with vehicle-treated controls (n = 9; -12%; p = 0.008). Furthermore, low-dose indapamide treatment resulted in a decrease of myocyte volume (59.0 +/- 10.6 vs. 79.0 +/- 9.8 m(3) x 10(-27); p < 0.05) and an improvement of molecular markers of hyper trophy: a reduction of LV atrial natriuretic factor mRNA expression (-37%; p < 0.05), and an increase of the V-1/V-3 myosin ratio (+121%; p < 0.05). Low-dose indapamide also reduced significantly plasma (-65%) and LV angiotensin-converting enzyme (ACE) activities (-74%) as well as LV mRNA levels (-24%). These changes were observed despite continued pressure overload of the LV and despite a lack of significant changes in sodium excretion with the prolonged administration of low-dose indapamide. High-dose indapamide treatment showed no significant effects on LV mass, structure, and gene expression. Furthermore, high-dose indapamide increased plasma renin activity substantially, whereas low-dose treatment was without effect on circulating renin. In conclusion, in rats with continuous LV pressure-overload low-dose treatment with indapamide leads to mild regression of cardiac hypetrrophy, accompanied by a downregulation of components of the cardiac renin-angiotensin system. These effects may be mediated by mechanisms apart from the known diuretic and antihypertensive actions of indapamide, because sodium excretion and blood pressure were stable with long-term treatment and are unlikely to be related to LVH regression in this model.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | ANGIOTENSIN-CONVERTING ENZYME; ESSENTIAL-HYPERTENSION; CARDIAC-HYPERTROPHY; AORTIC-STENOSIS; INHIBITION; HEARTS; CONTRACTILITY; RESPONSES; REVERSAL; SYSTEM; diuretic agent; hypertrophy; histology; rats; renin-angiotensin system |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Innere Medizin II |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 22 Mar 2022 15:33 |
| Last Modified: | 22 Mar 2022 15:33 |
| URI: | https://pred.uni-regensburg.de/id/eprint/42176 |
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