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Endothelium-dependent contraction produced by acetylcholine and relaxation produced by histamine in monkey basilar arteries

Life Sciences
Publication Date
DOI: 10.1016/0024-3205(93)90151-r


Abstract The present experiments were carried out to investigate endothelium-dependence of the responses to ACh, arachidonic acid and histamine in monkey basilar arteries. As we reported previously (1), ACh (10 −7 M) and arachidonic acid (5 × 10 −7 M) caused endothelium-dependent contraction (EDC) in both monkey and canine basilar arteries. The endothelium-derived contracting factor (EDCF) is probably TXA 2, since the EDC was attenuated by a cyclooxygenase inhibitor (aspirin, 5 × 10 −5 M), thromboxane A 2 (TXA 2) synthetase inhibitors (OKY-046, 10 −5 M; RS-5186, 10 −6 M) and TXA 2 antagonists (ONO-3708, 10 −8 M; S-145, 5 × 10 −9 M). Histamine caused endothelium-dependent relaxation (EDR) in monkey basilar arteries and EDC in canine basilar arteries. The EDR in monkey basilar arteries was attenuated by nitric oxide synthetase inhibitor, N G-monomethyl-L-arginine (L-NMMA) in a concentration-dependent manner and the EDC in canine basilar arteries was attenuated by aspirin, TAX 2 synthetase inhibitors and TXA 2 antagonists. The EDR and EDC were antagonized by tripelennamine (10 −6 M) but not by cimetidine (10 −5 M), indicating that they are mediated by H 1-receptors. From these results, we suggest that in the monkey basilar artery, either there are two types of endothelium, an EDCF type for ACh and arachidonic acid and an EDRF type for histamine, or there is single type of endothelium with two types of signalling processes, one for EDC and one for EDR.

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