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

<jats:p><jats:list list-type="explicit-label"> <jats:list-item><jats:p>Endothelin‐1 (ET‐1) caused a concentration‐dependent contraction of helical strips from rat thoracic aorta in the absence of extracellular Ca<jats:sup>2+</jats:sup>. The Ca<jats:sup>2+</jats:sup>‐depleted muscle strips, prepared by three repeated applications of 10<jats:sup>−2</jats:sup> <jats:sc>m</jats:sc> caffeine or 10<jats:sup>−6</jats:sup> <jats:sc>m</jats:sc> noradrenaline in Ca<jats:sup>2+</jats:sup>‐free buffer, were contracted by 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc> ET‐1 in the same manner as non‐treated strips.</jats:p></jats:list-item> <jats:list-item><jats:p>In the absence of extracellular Ca<jats:sup>2+</jats:sup>, 10<jats:sup>−7</jats:sup> <jats:sc>m</jats:sc> 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 60 min. Preincubation of the strips with 10<jats:sup>−7</jats:sup> <jats:sc>m</jats:sc> PMA for 60 min in Ca<jats:sup>2+</jats:sup>‐free buffer, did not affect the 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc> ET‐1‐induced contraction, but decreased the 5 × 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc> phorbol 12,13‐dibutyrate (PDB)‐, or the 10<jats:sup>−7</jats:sup> <jats:sc>m</jats:sc> PMA‐induced contraction, and potentiated the contraction induced by 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc> urotensin II. Preincubation with 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc> ET‐1 (which induced maximum contraction) for 25 min in Ca<jats:sup>2+</jats:sup>‐free buffer did not change the subsequent contraction induced by PMA (10<jats:sup>−7</jats:sup> <jats:sc>m</jats:sc>) or urotensin II (10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc>) but gave a somewhat lower maximum tension than in non‐treated strips.</jats:p></jats:list-item> <jats:list-item><jats:p>Calyculin‐A, a potent inhibitor of phosphatase, also induced a contraction of the Ca<jats:sup>2+</jats:sup>‐depleted muscle strips in Ca<jats:sup>2+</jats:sup>‐free buffer. Preincubation of the strips with ET‐1 (10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc>) or PMA (10<jats:sup>−7</jats:sup> <jats:sc>m</jats:sc>) decreased the calyculin‐A (3 × 10<jats:sup>−8</jats:sup> <jats:sc>m</jats:sc>)‐induced contraction.</jats:p></jats:list-item> <jats:list-item><jats:p>These results suggest that ET‐1 may induce phosphorylation of an unknown protein either without an increase in myoplasmic Ca<jats:sup>2+</jats:sup> concentration or, alternatively, with mobilization of intracellular Ca<jats:sup>2+</jats:sup> from noradrenaline‐ and caffeine‐insensitive Ca<jats:sup>2+</jats:sup> sources, through a mechanism different from that of phorbol ester.</jats:p></jats:list-item> </jats:list></jats:p>