Mechanisms of dexfenfluramine-induced vasoconstriction were studied in isolated pulmonary arteries suspended in organ baths for isometric tension recording. Dexfenfluramine (10-7-10-4 M) caused concentration-dependent contractions in rat and human pulmonary arteries with and without endothelium. In pulmonary arteries of the rat, the response to dexfenfluramine was nearly abolished by treatment with the α-adrenoceptor antagonists, phentolamine (10-6 M) or prazosin (10-7 M). In human pulmonary arteries, the concentration-response curve to dexfenfluramine was unaltered by the presence of phentolamine (10-6 M), prazosin (10-7 M), ketanserin (10-6 M), or indomethacin (3x10-6 M). The results suggest that dexfenfluramine causes contraction of pulmonary vascular smooth muscle by multiple mechanisms, one of which involves activation of α-adrenoceptors within the blood vessel wall. The mechanisms by which dexfenfluramine causes pulmonary vasoconstriction may differ between rat and human pulmonary arteries. Copyright (C) 2000.
|Original language||English (US)|
|Number of pages||6|
|Journal||European Journal of Pharmacology|
|State||Published - Aug 4 2000|
- Pulmonary arteries
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