Abstract
We investigated the nature of the contraction produced by 5-hydroxytryptamine (5-HT) in the rat pulmonary artery, and compared it with that produced in the rat aorta. Both ketanserin and ritanserin inhibited 5-HT-induced contraction in the pulmonary artery non-competitively. In contrast, ketanserin competitively antagonized the contraction in the aorta. Bunazosin, a selective alpha 1-blocker, partially inhibited 5-HT-induced contraction in the pulmonary artery, but not in the aorta. In both the pulmonary artery and aorta, 8-OH-DPAT, a 5-HT1A selective agonist, produced a concentration-dependent contraction. In the pulmonary artery, 5-HT and 8-OH-DPAT produced contractions with similar potencies. In contrast, 8-OH-DPAT was less potent than 5-HT in the aorta. Bunazosin inhibited 8-OH-DPAT-induced contraction in both vessels. However, pindolol, a 5-HT1A antagonist, did not inhibit 8-OH-DPAT-induced contraction in the pulmonary artery. These results suggest that 5-HT produces contraction via not only 5-HT2 receptor, but also non-5-HT2 receptor (probably alpha 1-adrenoceptor) in the rat pulmonary artery. Furthermore, 8-OH-DPAT does not activate the 5-HT1A receptor to produce a contraction, but does activate other receptors which interact with alpha 1-adrenoceptor.
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