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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.
P Caroni, and
L Reinlib, and
E Carafoli
May 1982,
The Journal of biological chemistry,
P Caroni, and
L Reinlib, and
E Carafoli
January 1987,
The American journal of physiology,
P Caroni, and
L Reinlib, and
E Carafoli
August 1987,
European journal of biochemistry,
P Caroni, and
L Reinlib, and
E Carafoli
March 1998,
The American journal of physiology,
P Caroni, and
L Reinlib, and
E Carafoli
August 1981,
FEBS letters,
P Caroni, and
L Reinlib, and
E Carafoli
November 1988,
Molecular and cellular biochemistry,
P Caroni, and
L Reinlib, and
E Carafoli
April 1990,
Archives of biochemistry and biophysics,
P Caroni, and
L Reinlib, and
E Carafoli
March 1988,
The American journal of physiology,
P Caroni, and
L Reinlib, and
E Carafoli
September 1988,
The American journal of physiology,
P Caroni, and
L Reinlib, and
E Carafoli
April 1988,
Biochimica et biophysica acta,
