Abstract
Electrical field stimulation (9 V, 1.0 ms, 4 Hz) of isolated segments of rat tail arteries and dog coronary arteries inhibits contractile responses to exogenous norepinephrine and elevated K concentration. This inhibitory effect of electrical stimulation is blocked by various agents that alter O2 metabolism: superoxide dismutase, catalase, glutathione, ascorbate and dimethyl sulfoxide. The inhibitory effect apparently is due to an action of O2 free radical metabolites that are generated by the electrical stimulation of the O2-rich buffer. These free radical metabolites have 2 actions: they oxidize drugs in the experimental system, and they exert a direct inhibitory action on vascular smooth muscle.

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