This Article Full Text Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Wolf, K. Articles by Kurtz, A. Search for Related Content PubMed PubMed Citation Articles by Wolf, K. Articles by Kurtz, A.

(Hypertension. 1995;26:1011-1017.)
© 1995 American Heart Association, Inc.

Articles

Renal Artery Stenosis Rapidly Enhances Atrial Natriuretic Peptide Gene Expression

Konrad Wolf; Armin Kurtz

From the Institut für Physiologie I, Universität Regensburg (Germany).

Correspondence to Konrad Wolf, PhD, Institut für Physiologie I, Universität Regensburg, D-93040 Regensburg, FRG. E-mail konrad.wolf@alf1.ngate.uni-regensburg.de.

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 substitu- tion, 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 gene expression. Moreover, our results suggest that activation of the 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.

Key Words: hypertrophy • renin-angiotensin system • furosemide • calcium antagonists

This article has been cited by other articles:

				W. Xiang, J. Kong, S. Chen, L.-P. Cao, G. Qiao, W. Zheng, W. Liu, X. Li, D. G. Gardner, and Y. C. Li Cardiac hypertrophy in vitamin D receptor knockout mice: role of the systemic and cardiac renin-angiotensin systems Am J Physiol Endocrinol Metab, January 1, 2005; 288(1): E125 - E132. [Abstract] [Full Text] [PDF]

				P. Sandner, M. Kornfeld, X. Ruan, W. J. Arendshorst, and A. Kurtz Nitric Oxide/cAMP Interactions in the Control of Rat Renal Vascular Resistance Circ. Res., February 5, 1999; 84(2): 186 - 192. [Abstract] [Full Text] [PDF]