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Department of Cardiology, Royal North Shore Hospital, and Department of Medicine, University of Sydney, St. Leonards, New South Wales 2065, Australia
Insulin enhances
Na+-K+ pump activity in various noncardiac
tissues. We examined whether insulin exposure in vitro regulates Na+-K+ pump function in rabbit ventricular
myocytes. Pump current (Ip) was measured using the
whole-cell patch-clamp technique at test potentials
(Vms) from 
100 to +60 mV. When the
Na+ concentration in the patch pipette
([Na]pip) was 10 mM, insulin caused a
Vm-dependent increase in Ip.
The increase was ~70% when Vm was at near
physiological diastolic potentials. This effect persisted after
elimination of extracellular voltage-dependent steps and when
K+ and K+-congeners were excluded from the
patch pipettes. When [Na]pip was 80 mM, causing
near-maximal pump stimulation, insulin had no effect, suggesting that
it did not cause an increase in membrane pump density. Effects of
tyrphostin A25, wortmannin, okadaic acid, or bisindolylmaleimide I in
pipette solutions suggested that the insulin-induced increase in
Ip involved activation of tyrosine kinase,
phosphatidylinositol 3-kinase, and protein phosphatase 1, whereas
protein phosphatase 2A and protein kinase C were not involved.
sodium-potassium-adenosinetriphosphatase; whole-cell voltage clamp; second messengers
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