Similarities of the in vivo and in vitro effects of mercuric chloride on [3H]ouabain binding and potassium activation of Na+/K(+)-ATPase in isolated rat cerebral microvessels.

A previous study revealed that a single i.p. administration of 6 mg/kg body wt. of mercuric chloride (MC) durably inhibits the rat cerebral microvascular Na+/K(+)-ATPase activity [1]. In this study, cerebral microvessels isolated 18 h after MC treatment were compared to those obtained from control rats and subsequently treated or not treated with MC in vitro, with regard to: (a) [3H]ouabain binding to, and (b) K(+)-activation kinetics of, the Na+/K(+)-ATPase. Microvessels from MC-treated rats showed a decrease of [3H]ouabain binding down to 62% of the control binding, and the same degree of inhibition was attained in microvessels treated in vitro with 5 microM MC. Analysis of the K(+)-activation kinetics of Na+/K(+)-ATPase revealed a decrease of Vmax from the control value of 13.1 to 7.67 mumol/mg/h in microvessels from MC-treated rats and 6.07 mumol/mg/h in microvessels treated in vitro with 5 microM MC, with no change in Km in either case. The similarity of the effects of in vivo and in vitro treatments suggests that the inhibition of the cerebromicrovascular Na+/K(+)-ATPase following in vivo administration of MC results from a direct interaction of Hg2+ with the enzyme.