Abstract
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) |
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Pages (from-to) | 229-234 |
Number of pages | 6 |
Journal | European Journal of Pharmacology |
Volume | 401 |
Issue number | 2 |
DOIs | |
State | Published - Aug 4 2000 |
Keywords
- Dexfenfluramine
- Indomethacin
- Ketanserin
- Phentolamine
- Prazosin
- Pulmonary arteries
ASJC Scopus subject areas
- Pharmacology