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Journal of Applied Physiology, Vol 76, Issue 5 1976-1982, Copyright © 1994 by American Physiological Society
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T. Fukuroda, M. Kobayashi, S. Ozaki, M. Yano, T. Miyauchi, M. Onizuka, Y. Sugishita, K. Goto and M. Nishikibe
Tsukuba Research Institute, Banyu Pharmaceutical Co., Japan.
We studied which endothelin (ET) receptor subtypes mediate ET-1-induced vasocontraction in the human pulmonary artery (PA) compared with the rabbit PA. ET-1 produced potent contraction in both human and rabbit isolated PAs. In human PA, ET-1-induced contraction was competitively antagonized by BQ-123 (an ETA receptor antagonist) with a pA2 value of 7.68. In rabbit PA, however, even a high concentration of BQ-123 (1 microM) did not affect the contraction. BQ-3020 (an ETB receptor agonist) produced potent contraction in rabbit PA but not in human PA. Binding assays of the membrane preparations showed that human and rabbit PAs contained ETA and ETB receptors in ratios of 93:7 and 23:77, respectively. These results suggest interspecies differences in the ET receptor subtypes that mediate ET-1-induced vasocontraction; ETA receptors are dominant in the human PA, whereas ETB receptors are dominant in the rabbit PA. Furthermore, the predominance of ETA receptors in human PA was supported by autoradiographical studies. If ET-1 acts as a physiological and/or pathophysiological vasocontractor in the human pulmonary circulation, an ETA receptor antagonist would function as a pulmonary vasodilator in humans.
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