DELLABRUNA, R and RIES, S and HIMMELSTOSS, C and KURTZ, A (1995) EXPRESSION OF CARDIAC ANGIOTENSIN-II AT(1) RECEPTOR GENES IN RAT HEARTS IS REGULATED BY STEROIDS BUT NOT BY ANGIOTENSIN-II. JOURNAL OF HYPERTENSION, 13 (7). pp. 763-769. ISSN 0263-6352,
Full text not available from this repository.Abstract
Objective: To examine the regulation by angiotensin II and by steroids of the expression of the angiotensin II AT(1a) and AT(1b) receptor genes in rat hearts. Methods: Endogenous levels of angiotensin II in the rats were increased either by unilateral 0.2-mm renal artery clips or by subcutaneous infusions of frusemide (12 mg/day) and by low-sodium diet. To inhibit endogenous angiotensin II actions the rats received the AT(1) receptor antagonist losartan (40mg/kg per day) or the angiotensin converting enzyme inhibitor ramipril (8 mg/kg per day). Circulating levels of glucocorticoids were elevated by subcutaneous injections of dexamethasone (400 mu g/kg per day) and levels of mineralocorticoids were increased by subcutaneous injections of deoxycorticosterone acetate (2 mg/kg per day). AT(1a) and AT(1b) messenger RNA (mRNA) levels were semiquantified by reverse-transcriptase polymerase chain reaction and related to actin mRNA. Results: The AT(1a) mRNA:AT(1b) mRNA ratio in the hearts of untreated rats was 10:1. Unilateral renal artery clipping led to a 30% decrease in AT(1a) mRNA, whereas treatment with frusemide, losartan or ramipril had no effect on the AT(1a) or AT(1b) mRNA levels. Rats fed a low-sodium diet showed a 37% increase in AT(1a) gene expression. Dexamethasone increased AT(1a) mRNA by 100% and AT(1b) mRNA by 300%, whereas deoxycorticosterone acetate treatment decreased AT(1a) mRNA levels to 30% of the control values. Conclusions: The present results suggest that the expression of the predominant cardiac AT(1a) receptor gene is not feedback-regulated by endogenous angiotensin II, whereas steroid hormones appear to be effective regulators, because glucocorticoids stimulate AT(1) receptor gene expression and mineralocorticoids inhibit it.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | TYPE-1A RECEPTOR; HYPERTROPHY; SUBTYPE; GLUCOCORTICOIDS; STIMULATION; ANTAGONISTS; SEQUENCE; GROWTH; CELLS; RENIN-ANGIOTENSIN SYSTEM; RECEPTOR SUBTYPE; LOW SODIUM; CLIP; MESSENGER RNA LEVEL |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:37 |
| URI: | https://pred.uni-regensburg.de/id/eprint/52456 |
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