We compared the pressor response to endothelin-1 (ET-1) with that of big endothelin-1 (big ET-1) in mesenteric arteries, hindquarters and lungs of rats. In these three preparations, both peptides caused a concentration-dependent increase in the perfusion pressure. The ratio of big ET-1 concentration to ET-1 concentration needed for causing the same pressor action is different between organs; i.e., a mesentery ≫ a hindquarter ≥ a lung. Exposure to phosphoramidon, a metalloproteinase inhibitor, significantly suppressed the pressor response to big ET-1, in a similar fashion. This suppression is likely to be due to the inhibition of phosphoramidon-sensitive endothelin converting enzyme, since the inhibitor does not suppress an action of ET-1. Apparently there is a difference in potency for phosphoramidon-sensitive vasoconstriction of big ET-1 between organs and presumably regional differences in the functional phosphoramidon-sensitive conversion of big ET-1 in vasculatures. © 1993.
Hisaki, K., Matsumura, Y., Fujita, K., Maekawa, H., Takaoka, M., & Morimoto, S. (1994). Differences in potency of big endothelin-1-induced pressor action in rat isolated perfused mesenteric artery, hindquarter and lung. Life Sciences, 54(4), 275–280. https://doi.org/10.1016/0024-3205(94)00817-5