[Effect of autonomic drugs on Na K adenosine triphosphatase activity in the heart and skeletal muscles]

Abstract

It has been found that ATP-ase activity increases considerably in the heart after intravenous administration of adrenaline, noradrenaline, phenylephrine (50 micrograms/kg), phentolamine, atropine, and also after vagotomy and adrenaline given after vagotomy. In the skeletal muscle ATP-ase activity increases considerably after noradrenaline, isoprenaline, phenylephrine (50 micrograms/kg), adrenaline given after phentolanine and Ach given after denervation of the muscle. A decrease in the activity of the enzyme in the heart was found after propranolol hexamethonium and Ach given after vagotomy, whereas in the skeletal muscle after Ach, hexamethonium and after muscle denervation. No changes or weak actions in the skeleton muscle are evoked by phenylephrine (10 micrograms/kg), propranolol, atropine, tubokurarine as well as adrenaline given after muscle denervation. In the heart, however, isoprenaline, Ach, adrenaline after propranolol, Ach after atropine and Ach after hexamethonium. A very low involvement of the enzyme studied in utilization of ATP reserves in the heart and skeletal muscle was found. However, of significant importance in this process may be the reactions catalized by extramembrane ATP-ases. The autonomic nervous system effects ATP-ase activity, and stimulation of beta-adrenergic receptor causes an increase in the enzyme activity in both muscles, whereas stimulation of the muskarine receptor decreases the enzyme activity in the heart. Moreover, it was found that stimulation of N2 receptor of the motor plate results in increased ATP-ase activity in the skeletal muscle. The present studies have not brought enough evidence accounting for participation of alpha-adrenergic receptor in regulation of the enzyme studied.