Abstract
Na/K pump current (I(pump)) and intracellular Na concentration (Na(i))
were measured simultaneously in voltage-clamped rabbit ventricular
myocytes, under conditions where Na(i) is controlled mainly by
membrane transport. Upon abrupt pump reactivation (after 10-12 min
blockade), I(pump) decays in two phases. Initially, I(pump) declines
with little Na(i) change, whereas the second phase is accompanied
by Na(i) decline. Initial I(pump) sag was still present at external
K = 15 mM, but prevented by Na(i) approximately 100 mM. Initial
I(pump) sag might be explained by subsarcolemmal Na(i) (Na(SL))
depletion produced by rapid Na extrusion and I(pump). Brief episodes
of pump blockade allowed Na(SL) repletion, since peak postblockade
I(pump) exceeded I(pump) at the end of previous activation (without
appreciably altered global Na(i)). The apparent K(m) for Na(i)
was higher for continuous I(pump) activation than peak I(pump) (14.1
+/- 0.2 vs. 11.2 +/- 0.2 mM), whereas that based on dNa(i)/dt matched
peak I(pump) (11.6 +/- 0.3 mM). Na(SL) depletion (vs. Na(i))
could be as high as 3 mM for Na(i) approximately 18-20 mM. A simple
diffusion model indicates that such Na(SL) depletion requires
a Na diffusion coefficient 10(3)- to 10(4)-fold below that expected
in bulk cytoplasm (although this could be subsarcolemmal only). I(pump)
integrals and Na(i) decline were used to estimate intracellular
Na buffering, which is slight (1.39 +/- 0.09).
- 12770918
- adaptation,
- animals,
- atpase,
- biological,
- calcium,
- capacitance,
- cardiac,
- cell
- cells,
- comparative
- computer
- cultured,
- diffusion,
- distribution,
- electric
- gov't,
- h.s.,
- heart
- intracellular
- membrane
- models,
- muscle
- myocytes,
- non-u.s.
- p.,
- p.h.s.,
- physiological,
- potentials,
- rabbits,
- rats,
- research
- sarcolemma,
- simulation,
- size,
- sodium,
- space,
- study,
- support,
- tissue
- u.s.
- ventricles,
- {n}a$^{+}$-{k}$^{+}$-exchanging
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