Transmembrane sodium movement and regulation of contraction in frog atrial muscle during the inotropic effect of veratrine.
In this study, voltage clamp experiments to determine membrane conductance changes revealed that veratrine slowed considerably inactivation of the Na system, thereby greatly increasing Na inward current. The contractile response (registered simultaneously with membrane currents) was closely related to this increase: applying tetrodotoxin (TXX) or Na-free (sucrose) Ringer's solution abolished the effect of veratrine on electrical and mechanical activity almost simultaneously. With Na-free (LiCl) Ringer's solution the effect of veratrine on membrane current was obtained, but the mechanical response was unchanged. Thus transmembrane movement of Na ions is involved in regulation of contraction during the inotropic effect of veratrine. As veratrine did not substantially change the slow Ca inward current, inotropic action seems dependent on some intracellular stores of Ca ions. The possibility that intracellular Na ions govern the amount of intracellular Ca ions available for the development of the inotropic effect of veratrine is discussed.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001001:Anura; D002118:Calcium / Q000502:physiology; D004553:Electric Conductivity; D066298:In Vitro Techniques; D009200:Myocardial Contraction / Q000187:drug effects*; D009206:Myocardium / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism* / Q000502:physiology; D013997:Time Factors; D014702:Veratrine / Q000494:pharmacology*
D012964:Sodium; D014702:Veratrine; D002118:Calcium