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

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