Hepatic sodium-potassium exchange induced by adrenomimetic amines.
The effects of catecholamines on hepatic K+ and Na+ movements were studied in anesthetized dogs by measuring systemic arterial and hepatic venous electrolyte composition following intraportal injections of adrenergic agonists. All catecholamines studied caused the initial loss and subsequent uptake of K+ by the liver. The loss of hepatic K+ was accompanied by an uptake of Na+ at a 1:1 ratio. This accumulation of Na+ continued, although at a slower rate, for at least 8 min. Epinephrine and norepinephrine were much more potent in these effects than either phenylephrine or isoproterenol. Neither alpha- nor beta-adrenergic blockade, singly or in combination, had an appreciable effect on the magnitude or duration of the observed ion shifts. It is concluded that the predominant effect of catecholamines is to produce a net accumulation of hepatic Na+, and that the mechanism governing hepatic ion movements is nonadrenergic as defined by stimulation by specific adrenergic agonists and inhibition by specific adrenergic antagonists.
Hepatic sodium-potassium exchange induced by adrenomimetic amines. The effects of catecholamines on hepatic K+ and Na+ movements were studied in anesthetized dogs by measuring systemic arterial and hepatic venous electrolyte composition following intraportal injections of adrenergic agonists. All catecholamines studied caused the initial loss and subsequent uptake of K+ by the liver. The loss of hepatic K+ was accompanied by an uptake of Na+ at a 1:1 ratio. This accumulation of Na+ continued, although at a slower rate, for at least 8 min. Epinephrine and norepinephrine were much more potent in these effects than either phenylephrine or isoproterenol. Neither alpha- nor beta-adrenergic blockade, singly or in combination, had an appreciable effect on the magnitude or duration of the observed ion shifts. It is concluded that the predominant effect of catecholamines is to produce a net accumulation of hepatic Na+, and that the mechanism governing hepatic ion movements is nonadrenergic as defined by stimulation by specific adrenergic agonists and inhibition by specific adrenergic antagonists.