EFFECTS OF CALCIUM ION ON THE RISING PHASE OF THE ACTION POTENTIAL IN RABBIT SINOATRIAL NODE CELLS

Akinori NOMA, Hiroshi IRISAWA
1976 The Japanese Journal of Physiology  
To clarify the role of Ca ion in the rising phase of the sinoatrial (S-A)node action potential,the sigmoidal relationship between the maximum rate of rise of the action potential and the maximum diastolic potential was examined at various concentrations of Ca.The membrane potential was changed by applying a current across a single sucrose gap.The sigmoidal curve shifted toward the positive potential without a change in maximum value when the Ca concentration was increased from nominal"zero"to
more » ... m nominal"zero"to 10mm.Therefore,it is concluded that Ca ion modifies the inactivation process of Na current which is responsible for the rapid rising phase of the S-A node action potential. The duration of the action potential and the maximum diastolic potential were decreased with an increase in Ca concentration.The observation that the overshoot of the action potential increased by 12 mV for a tenfold increase in concentration of Ca(within the range of 0.1-5.0 mm) suggests that the inward current of Ca ion may be responsible for the overshoot of the S-A node action potential. Ionic species responsible for the rising phase of the action potential of the sinoatrial(S-A) node cell are still a subject of controversy.The finding that the maximum rate of rise of depolarization is dependent upon both the extracellular concentration of sodium ion([Na]o) and the membrane potential (NoMA and IRISAWA,1974) supports the assumption that Na ion is responsible for the rapid rising phase of the action potential.However,the action potential of the S-A node cell is resistive to TTX(YAMAGISHI and SANO,1966),but is inhibited by Mn ion (LENFANT et al.,1968; BROOKS and Lu,1972).Therefore,the Ca ion may carry a part of the inward current in the S-A node action potential.If most of the inward current would be carried by the Ca ion,the highest value of the maximum
doi:10.2170/jjphysiol.26.93 fatcat:puc7uhwdpvcy7hqvdekpmdfvrm