K. Hisaki et al., DIFFERENCES IN POTENCY OF BIG ENDOTHELIN-1-INDUCED PRESSOR ACTION IN RAT ISOLATED-PERFUSED MESENTERIC-ARTERY, HINDQUARTER AND LUNG, Life sciences, 54(4), 1994, pp. 275-280
We compared the pressor response to endothelin-1 (ET-1) with that of b
ig endothelin-1 (big ET-1) in mesenteric arteries, hindquarters and lu
ngs of rats. In these three preparations, both peptides caused a conce
ntration-dependent increase in the perfusion pressure. The ratio of bi
g ET-1 concentration to ET-, 1 concentration needed for causing the sa
me pressor action is different between organs; i.e., a mesentery >> a
hindquarter greater-than-or-equal-to a lung. Exposure to phosphoramido
n, a metalloproteinase inhibitor, significantly suppressed the pressor
response to big ET-1, in a similar fashion. This suppression is likel
y to be due to the inhibition of phosphoramidon-sensitive endothelin c
onverting enzyme, since the inhibitor does not suppress an action of E
T-1. Apparently there is a difference in potency for phosphoramidon-se
nsitive vasoconstriction of big ET-1 between organs and presumably reg
ional differences in the functional phosphoramidon-sensitive conversio
n of big ET-1 in vasculatures.