SCHUNKERT, H and TANG, SS and LITWIN, SE and DIAMANT, D and RIEGGER, G and DZAU, VJ and INGELFINGER, JR (1993) REGULATION OF INTRARENAL AND CIRCULATING RENIN-ANGIOTENSIN SYSTEMS IN SEVERE HEART-FAILURE IN THE RAT. CARDIOVASCULAR RESEARCH, 27 (5). pp. 731-735. ISSN 0008-6363,
Full text not available from this repository.Abstract
Objective: Activation of the intrarenal renin-angiotensin system may contribute to the pathophysiology of heart failure by accelerating the generation of angiotensin II at local sites within the kidneys. Activation of the local intrarenal renin-angiotensin system occurs in rats and with mild heart failure. The aim of the present study was to examine components of the circulating as well as the intrarenal renin-angiotensin system in rats with severe heart failure. Methods: Six weeks after experimental myocardial infarction (heart failure, HF; n=8) or sham operation (control, C; n=6), haemodynamics and the circulating and intrarenal components of the renin-angiotensin system were studied. Results: HF rats were characterised by large infarctions (scar tissue >40% of the left ventricular circumference). In comparison to sham operated controls, large myocardial infarctions resulted in severe heart failure with decreased systolic [108(SEM 3) mm Hg v 132(3) in C; p<0.001] and diastolic arterial blood pressure [83(3) mm Hg v 95(2) in C; p<0.05], decreased left ventricular systolic pressure [109(3) mm Hg v 132(3) in C; p<0.0051 and increased left ventricular end diastolic pressure [27(2) mm Hg v 5(1) in C; p<0.0001]. In rats with severe heart failure, the circulating renin-angiotensin system was activated, with an increase in plasma renin activity (3.5-fold, p<0.05) and plasma angiotensin II concentration (threefold, p<0.01). In parallel, the intrarenal renin-angiotensin system was activated in severe heart failure. Increases occurred in renal renin mRNA level (1.7-fold, p<0.01), renal angiotensinogen mRNA level (1.8-fold, p<0.05), and renal angiotensin II concentration (twofold, p<0.05) compared to C. Intrarenal angiotensin II concentrations exceeded plasma levels by a factor of 50 and were positively correlated with renal angiotensinogen mRNA levels (r=0.874, p<0.001), suggesting that local synthesis is the major source of angiotensin II found in the kidney. Conclusions: The intrarenal renin-angiotensin system may be selectively activated in mild heart failure, while both circulating and intrarenal renin-angiotensin systems are induced as the extent of left ventricular function worsens.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | CONVERTING-ENZYME-INHIBITION; MESSENGER-RNA EXPRESSION; MYOCARDIAL-INFARCTION; ALDOSTERONE SYSTEM; SODIUM-EXCRETION; RENAL-FUNCTION; MECHANISMS; CAPTOPRIL; SURVIVAL; RELEASE; RENIN; ANGIOTENSINOGEN; ANGIOTENSIN-II; GENE EXPRESSION; KIDNEY; HEART FAILURE; RAT |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:42 |
| URI: | https://pred.uni-regensburg.de/id/eprint/53970 |
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