WOLF, K and KURTZ, A (1995) RENAL-ARTERY STENOSIS RAPIDLY ENHANCES ATRIAL-NATRIURETIC-PEPTIDE GENE-EXPRESSION. HYPERTENSION, 26 (6). pp. 1011-1017. ISSN 0194-911X, 1524-4563
Full text not available from this repository.Abstract
The aim of this study was to examine the influence of the systemic renin-angiotensin system on the gene expression of atrial natriuretic peptide in rat hearts. The renin-angiotensin system was stimulated (1) by unilateral renal artery clipping (0.2-mm clip, 2 days), producing a fourfold increase of circulating plasma renin activity and increasing blood pressure. (2) by furosemide infusion with simultaneous salt substitution, increasing plasma renin activity values to 45 ng angiotensin I/h per milliliter without changing blood pressure; or (3) by administration of the calcium antagonist amlodipine, which increased plasma renin activity values to 42 ng angiotensin I/h per milliliter and lowered blood pressure. Unilateral renal artery clipping increased atrial natriuretic peptide mRNA levels approximately 20-fold in the left ventricles and approximately twofold in the right ventricles and atria. Furosemide infusion had no effect on cardiac atrial natriuretic peptide mRNA levels, and in amlodipine-treated rats, cardiac atrial natriuretic peptide mRNA levels decreased to 30% of control values. The increase of atrial natriuretic peptide mRNA in the ventricles during renal artery clipping was blunted by the administration of the angiotensin-converting enzyme inhibitor ramipril, which also attenuated the blood pressure rise. In clipped rats amlodipine did not change elevated plasma renin activity values but abolished the rise of blood pressure and also attenuated the rise of atrial natriuretic peptide mRNA in the hearts. These findings indicate that an increase of the activity of the systemic renin-angiotensin system does not result in an obligatory change in cardiac atrial natriuretic peptide expression. Moreover, our results suggest that activation renin-angiotensin system by renal artery stenosis preferentially stimulates left ventricular atrial natriuretic peptide gene expression by an angiotensin II-dependent mechanism that could be associated with the induction of myocardial hypertrophy.
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | MYOSIN HEAVY-CHAIN; COMPLETE NUCLEOTIDE-SEQUENCE; FULL LENGTH CDNA; CARDIAC-HYPERTROPHY; MYOCARDIAL GROWTH; RAT; RELEASE; POLYPEPTIDE; MYOCYTES; HEART; HYPERTROPHY; RENIN-ANGIOTENSIN SYSTEM; FUROSEMIDE; CALCIUM ANTAGONISTS |
| Depositing User: | Dr. Gernot Deinzer |
| Last Modified: | 19 Oct 2022 08:37 |
| URI: | https://pred.uni-regensburg.de/id/eprint/52182 |
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