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We determined the effect of plasma obtained from rats treated with DOCA-salt for 6 and 28 days on sodium pump activity, measured as ouabain-sensitive Rb+ uptake in tail arteries from these rats. The effect of an electrolytic lesion in the area of the anteroventral third cerebral ventricle (AV3V) before DOCA-salt treatment was investigated in relation to the ability of plasma to inhibit vascular Na+ pump activity. Systolic blood pressures, plasma sodium and potassium concentrations, body weights and haematocrit were also measured. Six days after DOCA-salt treatment, there was a 22% suppression of vascular Na+ pump activity in these rats. This suppression was due to a plasma factor since plasma from these rats produced a similar degree of suppression in arteries isolated from untreated control rats. Furthermore, tail arteries from DOCA-salt rats treated for 6 days displayed normal Na+ pump activity when incubated in plasma from control rats or in Krebs-Henseleit buffer. There was no elevation of systolic blood pressure at the end of 6 days of treatment with DOCA-salt. Placement of an electrolytic brain lesion in the AV3V area before treatment with DOCA-salt abolished the ability of plasma to inhibit the vascular Na+ pump. Treatment with DOCA-salt for 28 days resulted in a significant increase in systolic blood pressure, a decrease in plasma potassium concentration, and a significant increase in vascular Na+ pump activity (26%). This elevation in pump activity appears to be due to a change in the artery rather than a stimulating factor in the plasma, since incubation of the arteries in both Krebs-Henseleit buffer and in plasma taken from control rats still resulted in increased Na+ pump activity. Our data indicate that, 6 days after DOCA-salt treatment there appears to be an inhibitor of the vascular Na+ pump in the plasma which is undetectable by bio-assay if the rats are lesioned in the AV3V region before this treatment. Twenty-eight days after DOCA-salt treatment, the vascular Na+ pump is stimulated; this is due not to a plasma factor, but to a change in the artery.