Sodium ion mediated regulation of Na/K-ATPase gene expression in vascular smooth muscle cells

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Abstract
To determine whether sympathetic nerve stimulation induces a significant potassium uptake in the myocardium, the changes in myocardial potassium balance, catecholamine release, lactate uptake, and oxygen consumption were recorded in eight anaesthetised open chest pigs during electrical stimulation of the right intermediate cardiac nerve at 10 Hz. Potassium concentrations were continuously measured by polyvinylchloride valinomycin minielectrodes in arterial and coronary sinus blood. Potassium concentration in coronary sinus blood fell to a nadir 0.42(0.21-0.61) mmol·litre−1 below control values (median and 95% confidence interval) and resulted in a peak potassium uptake of 65(38-102) μmol·min−1 100g−1 after 2.5(2.0-3.0) min, which correlated (r=0.94, p−1 when a stable potassium concentration difference between arterial and coronary sinus blood was reached after 5.5(4.25-6.50) min. Cardiac contractility (LV dP/dt), myocardial oxygen consumption, and lactate uptake rose from control to peak potassium uptake (p−1 at control to 2208(1159-5627) pg·ml−1 at peak uptake and from 15(11-19) pg·ml−1 to 85(64-230) pg·ml−1 respectively. Arterial noradrenaline increased from 29(19-41) pg·ml−1 to 374(176-640) pg·ml−1 and arterial adrenaline rose from 15(11-23) pg·ml−1 to 31(24-52) pg·ml−1 (p<0.001). It is concluded that sympathetic nerve stimulation induces a substantial myocardial potassium uptake in a dose dependent relation to cardiac noradrenaline release and alters the contractile and metabolic state of the heart substantially with only minor changes in arterial catecholamine concentration.

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