Charge movements during the Na+-Ca2+ exchange in heart sarcolemmal vesicles.
The Na+-Ca2+ exchange was studied in a highly purified vesicular preparation derived from heart sarcolemma. The initial velocity of the Na+-driven Ca2+ influx, which was monitored continuously with a specific electrode, was 15 nmol/mg of protein per sec; the total Ca2+-accumulation capacity was 80 nmol/mg of protein. The Na+-Ca2+ exchange generated a current that was compensated for by the uptake of tetraphenylphosphonium in (Ph4P+) (when the latter was present in the medium), the influx of K+, and the efflux of Cl-. The movements of Ph4P were followed with a specific electrode. Ca2+ in the concentration range 3-50 microM induced an increase in the permeability of the sarcolemmal membrane to K+. Under conditions of optimal charge neutralization by K+ (i.e., in the presence of valinomycin), the Km (Ca2+) of the exchanger was 1.5 microM. The Na+-Ca2+ exchange was inhibited by chlorpromazine and was not inhibited by vanadate.
D000818:Animals; D001693:Biological Transport, Active / Q000187:drug effects; D002118:Calcium / Q000378:metabolism*; D002474:Cell-Free System; D002746:Chlorpromazine / Q000494:pharmacology; D004285:Dogs; D009206:Myocardium / Q000378:metabolism*; D010539:Permeability; D011188:Potassium / Q000378:metabolism; D012508:Sarcolemma / Q000378:metabolism*; D012964:Sodium / Q000378:metabolism*; D014639:Vanadium / Q000494:pharmacology
D014639:Vanadium; D012964:Sodium; D011188:Potassium; D002118:Calcium; D002746:Chlorpromazine