m value, from -90 mV begins to drop and approaches -60 mV At Vm value of-60 mV, all the m gates (which are nol yet open) open simultaneously —

Na+ entry is now at a massive rate — very rapid depolarization (phase 0) Now, the h gates close the Na channels (fig 5.29) — Na+ influ" ceases and O- mflui occurs— Vm value, now from +30 rnV begins lo fall When the Vrn is about -30 mV. another type of channels, called slaw calcium channels open up (incidentally, the channels which opened due to opening up of m gates are called "fasit sodium channels") When the slaw channels open, they admit NO as well as Ca++ Phase 2 is thus; mainly due lo Ci++ entry via slow calcium channels Phase 3 is due to, (i) closure of slow cha- nnels which were admitting Ca++, and (ii) expulsion of K+ from ICF by opening the K+ channels [ NB m and h. these two names are used following Hodgkm and Hurley's nomenclature and hence they should be retained) Interrelationship between Na+and Ca++ Recall, (i) after each action potential (AP), some Na+ accumulate and some K+ are lost from the inside of the can. To correct this. Na+ K+ ATPase (= Na pump), present in the cell membrane works and intrudes m value, from -90 mV begins to drop and approaches -60 mV At Vm value of-60 mV, all the m gates (which are nol yet open) open simultaneously —the extra Na+ and draws in the K+ [chap 2 sec I) ( ii ) also concentration of free Ca++ inside the cell, [Ca++i is very low and that in the ECF high. During an AP in myocardial cell, the C*++]i rises because, (a) Ca++ enter from ECF in phase 2 of AP. and (b) Ca++released (from the stores) from the L tubules (= sarcoplasrnic reticulum) Obviously this excess of frt* Ca++ must be removed, otherwise a prolonged cardiac contraction (a disaster) will result .This is done by (a) reuptake of Ca++ by the L tubules, and (b) through an exchange system called Na - Ca exchanger Actually this exchange system is a channel through the cell membrane (sarcolemma), when open it communicates between the ECF and the ICE Ca++ are driv­en out (against concentration and electrical gradient) to the ECF and m exchange Na+ are drawn in from the ECF The energy required for ihis operation comes from hydrolysis of ATP by the help of Na+ K+ ATPase of The cell membrane Conclusion is. inhibition of Na+ K+ ATPase Ca++ accumulation within the cell. Digitalis (a popular drug m the treatment of cardiac failure) inhibits Na+ K+ATPase -* causes intracelllular Ca++ accumulation -- raises myocardial contraclrlity. Applied physiology. The slow channels, which admit C a++ (and there fore cause prolongation of the state of partial depolarization in .Cardiac