Ishizuka N, Berlin J R
Bockus Research Institute, Graduate Hospital, Philadelphia, PA 19146.
Pflugers Arch. 1993 Aug;424(3-4):361-3. doi: 10.1007/BF00384364.
Na pump current was measured in rat ventricular myocytes to determine if beta-adrenergic stimulation can directly modulate Na,K-ATPase activity. Enzymatically-isolated heart cells were voltage-clamped with a single patch electrode and Na pump current was briefly activated by rapidly increasing extracellular [K+] from 0 to 15 mM for 3-5 s after other ionic currents were blocked or inactivated. The salt solution in the voltage-clamping electrode included (in mM): (1) 100 Na+, 10 EGTA, (2) 5 Na+, 10 EGTA, or (3) 100 Na+, 7.5 Ca2+, 10 EGTA (free [Ca2+] = 480 nM). With all three electrode solutions, Na pump current was not significantly changed after 2-4 min in the presence of 10 microM isoprenaline. beta-adrenergic pathways were still intact as evidenced by the two-fold increase in Cd(2+)-sensitive Ba2+ current through calcium channels that was observed in the presence of isoprenaline. Thus, beta-adrenergic stimulation does not appear to directly regulate Na,K-ATPase activity in rat ventricular myocytes.