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Serotonin receptor as a potential therapeutic target for pulmonary vascular remodeling
Author(s) -
Wang Huailiang
Publication year - 2003
Publication title -
drug development research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.582
H-Index - 60
eISSN - 1098-2299
pISSN - 0272-4391
DOI - 10.1002/ddr.10133
Subject(s) - vasoconstriction , hypoxic pulmonary vasoconstriction , pulmonary hypertension , pulmonary artery , receptor , vasodilation , serotonergic , agonist , 5 ht receptor , endocrinology , medicine , serotonin , pharmacology
Pulmonary hypertension can be caused in most mammalian species by numerous serotonergic drugs. That the 5‐HT 1B/1D ‐receptor agonist sumatriptan demonstrated a potent vasopressor response in the pulmonary circulation in human subjects suggests that the 5‐HT 1B/1D receptor may be involved in the vasoconstriction of human pulmonary arteries. Both 5‐HT 1B ‐ and 5‐HT 1D ‐receptor mRNA exist in the trigeminal ganglion. Only 5‐HT 1B receptor mRNA expression was detected in pulmonary artery smooth muscle. A higher level of 5‐HT 1B receptor mRNA expression existed in the pulmonary artery from the monocrotaline‐induced chronic pulmonary hypertensive rat, which was found to be associated with a higher vasoconstrictor effect to 5‐HT. The 5‐HT 1B receptor mediates pulmonary vasoconstriction and the enhanced expression of 5‐HT 1B receptor mRNA is closely related to the augmentation of 5‐HT‐induced pulmonary vasoconstriction. Therefore, serotonin may be a mediator of pulmonary hypertension via 5‐HT 1B receptor‐induced pulmonary vasoconstriction. The enhanced expression of 5‐HT 1B receptor mRNA is closely related to the augmentation of 5‐HT‐induced pulmonary vasoconstriction, suggesting that the 5‐HT 1B receptor is one of the important mechanisms of pulmonary hypertension; this may provide a novel and potential therapeutic target for this disease. Drug Dev. Res. 58:69–73, 2003. © 2003 Wiley‐Liss, Inc.