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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Nonpeptide endothelin receptor antagonists attenuate the pressor effect of diaspirin-crosslinked hemoglobin in rat.
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Nonpeptide endothelin receptor antagonists attenuate the pressor effect of diaspirin-crosslinked hemoglobin in rat.

机译：非肽内皮素受体拮抗剂减弱了diaspirin交联的血红蛋白对大鼠的加压作用。

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摘要

Endothelin 1 (ET-1) is a potent vasoactive and mitogenic peptide that is thought to participate in the hemodynamic effects elicited by drugs that block the biosynthesis and release of endothelium-derived nitric oxide (NO), such as NO synthase inhibitors. Using the nonpeptide endothelin receptor antagonists bosentan and LU-135252, we tested the hypothesis that endothelins contribute to the pressor activity of diaspirin-crosslinked hemoglobin (DCLHb), a hemoglobin-based oxygen carrier, whose pressor activity in mammals is attributed primarily to a scavenging action towards NO. The NO synthase inhibitor nitro-L-arginine methyl ester (L-NAME), ET-1, and noradrenaline (NA) were used as reference drugs. Bosentan markedly reduced the pressor effects elicited by DCLHb, L-NAME, and ET-1, but not those evoked by NA. LU-135252 attenuated the pressor effect elicited by DCLHb and ET-1, but not that produced by L-NAME or NA. The decreases in heart rate associated with the pressor effect of DCLHb and L-NAME were reduced by LU-135252, whereas only those elicited by DCLHb were attenuated by bosentan. In contrast with bosentan, LU-135252 caused a decrease in the baseline blood pressure and heart rate. These results suggest that endothelins may participate in the pressor activity of DCLHb. They suggest also that nonpeptide endothelin receptor antagonists such as bosentan or LU-135252 may be useful to counteract endothelin-mediated undesirable hemodynamic effects of drugs that inhibit the activity of the NO system.
机译：内皮素1（ET-1）是一种有效的血管活性和促有丝分裂肽，被认为参与阻断内皮源性一氧化氮（NO）的生物合成和释放的药物（如NO合酶抑制剂）引起的血液动力学作用。使用非肽内皮素受体拮抗剂波生坦和LU-135252，我们测试了以下假设：内皮素有助于泛美素交联的血红蛋白（DCLHb）（一种基于血红蛋白的氧气载体）的升压活性，其在哺乳动物中的升压活性主要归因于清除采取行动NO合酶抑制剂硝基L-精氨酸甲酯（L-NAME），ET-1和去甲肾上腺素（NA）用作参考药物。波生坦明显降低了DCLHb，L-NAME和ET-1引起的升压作用，但不降低NA引起的升压作用。 LU-135252减弱了DCLHb和ET-1引起的升压作用，但不减弱L-NAME或NA产生的升压作用。 LU-135252降低了与DCLHb和L-NAME的升压作用相关的心率降低，而波森坦减弱了仅DCLHb引起的心率降低。与波生坦相反，LU-135252导致基线血压和心率降低。这些结果表明内皮素可能参与了DCLHb的加压活性。他们还暗示，非肽内皮素受体拮抗剂（例如波生坦或LU-135252）可用于抵消内皮素介导的抑制NO系统活性的药物的不良血液动力学效应。

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