Inhibitory effects of cadmium ion on extracellular Ca2+-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 μM) or verapamil (1 μM), was markedly inhibited by CdCl₂ (0.1 mM). In the medium without Ca²⁺, phenylephrine (10 μM) induced a phasic contraction, which was markedly inhibited by CdCl₂ (0.1 mM)/ In the medium without Ca²⁺, phorbol 12-myristate 13-acetate (1 μM) and okadaic acid (10 μM) caused tonic contractile responses, which were strongly attenuated by CdCl₂ (0.1 mM) pretreatment. Contractile response to sodium fluoride (5 ∼ 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 Ca²⁺-independent component of agonist-induced vasoconstriction by hindering an intracellular contractile mechanism(s).