To evaluate the possibility for stimulation of Ca2+-activated K+ channels,
marine fish erythrocytes were incubated at 20-22 degreesC in saline contain
ing Ca2+-ATPase inhibitor (orthovanadate), Ca2+ ionophore (A23187), propran
olol or Pb2+, The intracellular K+ and Na+ concentrations were unchanged wh
en the cells were incubated up to for 2 h under control conditions and in t
he presence of 5 mM NH4VO3 and 1 mM Ca2+, About 50% cellular K+ was lost fr
om erythrocytes incubated in the presence of 0.01 mM A23187, 1 mM EGTA and
0.4-1.0 mM Ca2+, There was a significant loss of cellular K+ after addition
of 0,05-0.2 mM propranolol to incubation medium, The stimulatory effect of
propranolol on K+ efflux was independent of external Ca2+, Blockers. of Ca
2+ transport, verapamil and Co2+, caused only a small decrease in the K+ lo
ss induced by propranolol, The treatment of red cells with 1-2 muM Pb2+ led
to a small K+ efflux but they lost about 70% cellular K+ at Pb2+ concentra
tion of 20-50 muM. The K+ efflux induced by propranolol or Pb2+ was complet
ely blocked by 1 mM quinine, The stimulatory K+ loss from fish erythrocytes
was accompanied by only a small increase in intracellular Na+ concentratio
n. The data obtained indicate the possibility for induction of Ca2+-activat
ed and Pb2+-activated potassium channels in erythrocytes of marine fish.: I
t should be noted that the cells exhibit high sensitivity to propranolol, w
hich leads to activation of K+ channels without external Ca2+.