Contraction of rat thoracic aorta strips by endothelin‐1 in the absence of extracellular Ca²⁺

Abstract

1 Endothelin-1 (ET-1) caused a concentration-dependent contraction of helical strips from rat thoracic aorta in the absence of extracellular Ca2+. The Ca2+-depleted muscle strips, prepared by three repeated applications of 10-2M caffeine or 10-6M noradrenaline in Ca2`-free buffer, were contracted by 10-8MET-1 in the same manner as non-treated strips. 2 In the absence of extracellular Ca2 10 -7M phorbol 12-myristate 13-acetate (PMA), an activator of protein kinase C, induced a small but sustained contraction of the rat thoracic aorta strips within 60min.Preincubation of the strips with 10-7M PMA for 60min in Ca2'-free buffer, did not affect the 10-8M ET-1-induced contraction, but decreased the 5 x 10-8M phorbol 12,13-dibutyrate (PDB)-, or the 10-7M PMA-induced contraction, and potentiated the contraction induced by 10-8M urotensin II. Preincubation with 10-8M ET-1 (which induced maximum contraction) for 25min in Ca2+-free buffer did not change the subsequent contraction induced by PMA (10-7M) or urotensin II (10-8M) but gave a somewhat lower maximum tension than in non-treated strips. 3 Calyculin-A, a potent inhibitor of phosphatase, also induced a contraction of the Ca2+-depleted muscle strips in Ca2 '-free buffer. Preincubation of the strips with ET-1 (10-8M) or PMA (10-7M) decreased the calyculin-A (3 x 10 8 minduced contraction. 4 These results suggest that ET-1 may induce

Differential vasoconstrictor activity of human urotensin‐II in vascular tissue isolated from the rat, mouse, dog, pig, marmoset and cynomolgus monkey

“…In accord with previous studies performed using the goby isoform of U-II in ®sh, amphibian and mammalian (rat and rabbit aortae) isolated vascular tissue (Muramatsu et al, 1979;Gibson, 1987;Gibson et al, 1988;Itoh et al, 1987;1991;Conlon et al, 1996), potent, sustained and e cacious vasoconstriction was observed upon exposure of speci®c rat, dog, pig and primate isolated blood vessels to the human isoform of U-II (Table 5). Indeed, human U-II was between 8 and 109 fold more potent than ET-1.…”

“…This hypothesis is supported by the recent identi®cation of U-II isopeptides in the rat, mouse, pig and man (Ames et al, 1999;Coulouarn et al, 1998;Mori et al, 1999). The present study has evaluated the functional activity of human U-II in a range of native vascular tissue isolated from a variety of mammals.In accord with previous studies performed using the goby isoform of U-II in ®sh, amphibian and mammalian (rat and rabbit aortae) isolated vascular tissue (Muramatsu et al, 1979;Gibson, 1987;Gibson et al, 1988;Itoh et al, 1987;1991;Conlon et al, 1996), potent, sustained and e cacious vasoconstriction was observed upon exposure of speci®c rat, dog, pig and primate isolated blood vessels to the human isoform of U-II (Table 5). Indeed, human U-II was between 8 and 109 fold more potent than ET-1.…”

Eicosanoid‐induced Ca2+ release and sustained contraction in Ca2+‐free media are mediated by different signal transduction pathways in rat aorta

“…This would raise the possibility that the mechanism involved in the eicosanoid-induced sustained contractions is unrelated to the PKC that is activated by application of P-TPA. Similar synergism with P-TPA was obtained with urotensin II (Itoh et al, 1991). On the other hand, the prior short-term treatment with P-TPA resulted in attenuation of IP3 production and Ca2+…”

Investigations of the dual contractile/relaxant properties showed by antioquine in rat aorta

“…Autoradiographic and electron microscopic studies have confirmed that diltiazem, verapamil and dihydropyridines all accumulate within the mitchondrial matrix (Sato et al, 1971;Nakajima et al, 1975;Lullman et al, 1979;Pang & Sperelakis, 1983;Tagami et al, 1985) (Salaices et al, 1990;Itoh et al, 1991), or via phosphatase inhibition. With respect to the latter mechanism, it should be noted that two known potent inhibitors of type 1 and type 2A phosphatases, okadaic acid and calyculin-A (Ishihara et al, 1989;Obara et al, 1989), induce a similar contraction of smooth muscle, which is also independent of extracellular calcium.…”