The effects of N,N-diethyl-5-methyl[1,2,4]triazolo[1,5-α]pyrimidine-7-amine (trapidil) on the electrical activities of canine right ventricular muscle were studied using standard microelectrode techniques. Trapidil (10-4 and 10-3 mol/l) increased the plateau amplitude and shortened the duration of the action potential without changing the resting membrane potential and the maximum rate of rise of the action potential. Trapidil (10-3 mol/l) restored regenerative action potentials (the slow response) in the ventricular muscle depolarized by elevation of extra-cellular K+ concentrations to 30 mol/l. The slow response induced by trapidil was not affected by pindolol (10-7 mol/l) which abolished that elicited by isoprenaline (10-6 mol/l). These results indicate that the action of trapidil on the cardiac cell membrane is to increase the slow inward current during the action potential independently of stimulation of β-adrenoceptors. Taken together with the results obtained by previous investigations the present results suggest that the increase in slow inward current during the action potential would be responsible for the positive inotropic effect of trapidil and would probably be related to its inhibitory action on cyclic AMP phosphodiesterase.
|Number of pages||4|
|Publication status||Published - 1980 Jan 1|
ASJC Scopus subject areas
- Drug Discovery