THE N-3 POLYUNSATURATED FATTY ACID EICOSAPENTANOIC
ACID (EPA) STIMULATES THE NA-K PUMP IN RABBIT CARDIAC MYOCYTES. A.D. Pitt*, C. Fernandes, H.H. Rasmussen and
D.W. Whalley. Cardiology Dept. Royal North Shore Hospital,
Sydney, NSW. Acute
exposure of heart cells to fish oils, including EPA, has been shown to have
antiarrhythmic effects including reduction of beating rate, hyperpolarisation
of resting potential, and increase in threshold potential. Most studies have focused on the role of ion
channels in mediating this effect.
However, the influence of EPA on the Na-K pump has not been examined
despite the importance of this enzyme in determining contractility and membrane
potential. Methods:
Whole cell patch clamping was conducted on cardiac myocytes isolated
from rabbits. Na+K+
pump current (Ip) was measured using pipette Na+
concentrations ([Na]pip) of 10 mM (near physiological intracellular
levels) and 80 mM (to induce maximum Ip). Ip was defined as the shift in holding current upon
exposure to 100 mM ouabain
after 5-6 minutes superfusion with 5 mM EPA or control Tyrodes solution.
To assess the involvement of Na+ influx into the cell we used
a Na+-free superfusate. Results: (pA/pF, mean ±
SEM). EPA superfusion stimulated Ip at [Na]pip of 10 mM
(0.48 ± 0.04 vs control 0.32 ±
0.01, p<0.01) whilst maximal Ip at [Na]pip of 80 mM,
did not change with EPA superfusion (2.01 ± 0.10
vs control 2.03 ± 0.08). Pump stimulation by EPA
was still evident in the absence of extracellular Na, indicating that this effect
is independent of Na influx (0.50 ± 0.03
vs control 0.36 ± 0.04, p<0.05). Conclusion:
Acute EPA superfusion stimulates Ip via a shift in the apparent
affinity of the Na-K pump for intracellular Na. Na-K pump stimulation is expected to contribute to the
hyperpolarization of resting potential observed during exposure to EPA.
