Inhibitory effects of cadmium ion on extracellular Ca(2+)-independent contraction of rat aorta.

In vitro effects of cadmium ion on vasoconstriction, particularly on vasoconstriction independent of extracellular Ca2+, were investigated using isolated rat aorta. Aorta incubation with CdCl2 (0.01, 0.1 mM) significantly attenuated contractile responses to KCl and phenylephrine in the medium containing normal Ca2+ (2.5 mM). The contractile response to phenylephrine in the presence of calcium channel antagonists, nifedipine (1 microM) or verapamil (1 microM), was markedly inhibited by CdCl2 (0.1 mM). In the medium without Ca2+, phenylephrine (10 microM) induced a phasic contraction, which was markedly inhibited by CdCl2 (0.1 mM). In the medium without Ca2+, phorbol 12-myristate 13-acetate (1 microM) and okadaic acid (10 microM) caused tonic contractile responses, which were strongly attenuated by CdCl2 (0.1 mM) pretreatment. Contractile response to sodium fluoride (5 approximately 15 mM) in the absence of extracellular Ca2+ was strongly attenuated by CdCl2 (0.1 mM) pretreatment. These results suggest that cadmium ion depresses an extracellular Ca(2+)-independent component of agonist-induced vasoconstriction by hindering an intracellular contractile mechanism(s).