This Article Full Text (PDF) 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 Mortensen, L. H. Articles by Fink, G. D. Search for Related Content PubMed PubMed Citation Articles by Mortensen, L. H. Articles by Fink, G. D.

Hypertension, Vol 19, 676-680, Copyright © 1992 by American Heart Association

ARTICLES

Captopril prevents chronic hypertension produced by infusion of endothelin-1 in rats

LH Mortensen and GD Fink
Department of Pharmacology and Toxicology, Michigan State University, East Lansing 48824.

Endothelin-1 (ET-1), a potent vasoconstrictor peptide synthesized by the vascular smooth muscle endothelium, has been previously shown to produce a sustained, salt-sensitive elevation in mean arterial pressure when chronically infused over a 7-day period into male Sprague-Dawley rats. In addition to other physiological actions, ET-1 has been shown to have potent effects on various renal functions, including renin production. Activation of the renin-angiotensin system, therefore, may contribute to the pressor response induced by ET-1. In this investigation, captopril ([2S]-1-[3-mercapto-2-methylpropionyl]-L- proline), a sulfhydryl-containing angiotensin I converting enzyme inhibitor, was chronically administered to endothelin-infused rats to elucidate the role of the renin-angiotensin system in this animal model of hypertension. Rats were catheterized, housed in metabolic cages, and maintained on a fixed 6.0 meq.day-1 sodium intake throughout the experiment, with daily measurements taken of mean arterial pressure, heart rate, water intake, urine output, and urinary sodium and potassium excretions. Infusion of ET-1 alone at a rate of 5.0 pmol.kg- 1.min-1 for 7 days was associated with a significant and sustained increase in mean arterial pressure; concomitant chronic administration of captopril in another group of rats at a rate of 1.0 mg.kg-1.hr-1 prevented the ET-1-induced hypertension. In an additional study, however, increases in plasma angiotensin II concentration were not observed in rats administered ET-1 alone at 5.0 pmol.kg-1.min-1. These results indicate that endothelin-induced hypertension may involve stimulation of the renin-angiotensin system but not an increase in circulating angiotensin II concentration.

This article has been cited by other articles:

				A. A. Elmarakby, P. Morsing, and D. M. Pollock Regulation of Cardiovascular Signaling by Kinins and Products of Similar Converting-Enzyme Systems: Enalapril attenuates endothelin-1-induced hypertension via increased kinin survival Am J Physiol Heart Circ Physiol, June 1, 2003; 284(6): H1899 - H1903. [Abstract] [Full Text] [PDF]

				P. Moreau Endothelin in hypertension: A role for receptor antagonists? Cardiovasc Res, September 1, 1998; 39(3): 534 - 542. [Abstract] [Full Text] [PDF]

				G. S. Potter, R. J. Johnson, and G. D. Fink Role of Endothelin in Hypertension of Experimental Chronic Renal Failure Hypertension, December 1, 1997; 30(6): 1578 - 1584. [Abstract] [Full Text]

				K. A. H. Kaasjager, H. A. Koomans, and T. J. Rabelink Effectiveness of Enalapril Versus Nifedipine to Antagonize Blood Pressure and the Renal Response to Endothelin in Humans Hypertension, April 1, 1995; 25(4): 620 - 625. [Abstract] [Full Text]

				S. A. Douglas, M. Gellai, M. Ezekiel, G. Z. Feuerstein, J. D. Elliott, and E. H. Ohlstein Antihypertensive Actions of the Novel Nonpeptide Endothelin Receptor Antagonist SB 209670 Hypertension, April 1, 1995; 25(4): 818 - 822. [Abstract] [Full Text]