Abstract |
The role of cardiac endothelin-1 (ET-1) was studied by determining endogenous tissue and coronary ET-1 levels in isolated rat hearts. Hearts were perfused in an upside-down position with a colloid-free buffer and immunoreactive ET-1 was determined in timed collections of coronary effluent (E) and interstitial fluid (transudate, T) produced by the ventricles and appearing on their surface. Basal ET-1 concentrations were 0.2 +/- 0.01 pg/ml (T) and 0.03 +/- 0.002 pg/ml (E), i.e., the T:E concentration ratio was 7. Angiotensin II (0.1 mumol/L) or thrombin (5 U/ml) increased coronary perfusion pressure and ET-1 secretion but had no effect on the T:E ET-1 concentration ratio (5 and 9). In two different protocols of ischemia/reperfusion, T and E concentrations increased up to two- and fivefold, respectively. The T:E ratios were approximately 2, and the highest concentrations in either fluid were < 1 pg/ml. No change in coronary perfusion pressure was observed. In the presence of the ET-1-converting enzyme inhibitor phosphoramidon (1.7 mumol/L), ischemia-induced increases of ET-1 concentrations were attenuated in parallel with a time-dependent rise in coronary perfusion pressure. Therefore, under normoxic conditions and in ischemia/reperfusion, ET-1 is an endogenous vasodilator in the rat heart.
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Authors | F Brunner |
Journal | Journal of cardiovascular pharmacology
(J Cardiovasc Pharmacol)
Vol. 26 Suppl 3
Pg. S44-6
( 1995)
ISSN: 0160-2446 [Print] United States |
PMID | 8587439
(Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
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Chemical References |
- Endothelins
- Glycopeptides
- phosphoramidon
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Topics |
- Animals
- Endothelins
(analysis, physiology)
- Glycopeptides
(pharmacology)
- Myocardial Ischemia
(metabolism)
- Myocardium
(chemistry)
- Rats
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