Abstract

A possible mechanism for the pressor effect of cadmium was investigated in isolated rat thoracic aorta. Cadmium produced contractions at low concentrations, but relaxations at high concentrations. Phentolamine, a sympathetic alpha blocking agent did not inhibit the cadmium-induced contractions. These contractions were reduced in accordance with the decrease in Ca content in medium and were abolished in Ca-free medium, rather inducing a small degree of relaxation. When low concentrations of cadmium were applied repeatedly for a short period of time, the contractions were remarkably reduced and finally abolished. Noradrenaline-induced contractions were not affected after the completion of cadmium-tachyphylaxis. Low concentrations of cadmium potentiated K-, Ba- and noradrenaline-induced contractions, while high concentrations suppressed them. These results suggest that cadmium-induced contractions are dependent on external Ca and that they are produced by direct stimulation on the cell membrane. In addition, low concentrations of cadmium accelerate Ca availability, while high concentrations inhibit it.

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