Cardiovascular responses to the intravenous (i.v.) and the intracerebroventricular (i.c.v.) administration of cadmium acetate were evaluated in rats anaesthetized with urethane. Cadmium acetate (1 mg/kg i.v.) caused an initial fall followed by a persistent rise in blood pressure. Cadmium acetate (1 microgram i.c.v.) produced a more marked hypertensive effect. In the spinal-transected rat, the effect of intravenous cadmium was reduced but the effect of intraventricularly administered cadmium was completely abolished. It is, therefore, suggested that both central and peripheral mechanisms are involved in the pressor response to cadmium exposure.
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