(Na+, K+)-adenosine triphosphatase regulation by the sympathetic nervous system: effects of noradrenergic stimulation and lesions in vivo

Abstract

Effects of noradrenergic stimulation and depletion on the K+-p-nitrophenylphosphatase activity and ouabain binding associated with (Na+, K+)-adenosine triphosphatase (E.C. 3.6.1.3) were examined in heart, soleus, brown adipose tissue and kidney. Stimulation by repeated yohimbine or d-amphetamine increased and depletion by parenteral 6-hydroxydopamine decreased enzyme activity or ouabain binding in each tissue studied except kidney. Some increase in the parameters associated with (Na+, K+)-adenosine triphosphatase was seen after repeated doses of 1 mg/kg of d-amphetamine or yohimbine, with maximal effects at 2 mg/kg of yohimbine and 5 or 10 mg/kg of d-amphetamine. Stimulation was reduced by administration of alpha-1 or beta noradrenergic antagonists. Repeated treatment with isoproterenol, but not with phenylephrine, increased ouabain binding and enzyme activity in the heart. The decrease and recovery of enzyme activity in the heart after administration of the reversible noradrenergic neurotoxin N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4) were parallel to the recovery of norepinephrine content and desmethylimipramine binding. The effects of the noradrenergic changes appeared to involve chiefly the fraction of enzyme with high affinity for ouabain.