AJP - Cell Physiology, Vol 253, Issue 2 C253-C262, Copyright © 1987 by American Physiological Society
[Na]i modulates isoproterenol's effect on Ca permeability in cultured heart cells
D. Kim and T. W. Smith
Isoproterenol (ISO) augments the slow inward Ca current in cardiac muscle
cells. We examined the role of intracellular Na (Nai) on ISO-mediated
alterations in Ca uptake in cultured chick heart cells. In 140 mM Na
medium, 1 microM ISO did not measurably alter 45Ca uptake. When cells were
first preincubated in Na-free medium for 5 min and then incubated in
control medium with 45Ca, ISO increased 45Ca uptake by 30%. Nifedipine (10
microM), verapamil (1 microM), or dl-propranolol (1 microM) abolished the
effect of ISO on 45Ca uptake. CGP 28392 (1 microM), a Ca channel agonist,
increased Ca influx in a manner that was augmented by decreased Nai,
similar to the ISO response. Neither ISO nor CGP 28392 altered 45Ca uptake
when cells preincubated in Na-free medium were further incubated in Na-free
medium containing 45Ca. Exposure of cells to Na-free medium or 25 mM K+
medium caused depolarization of the resting membrane potential to
approximately -40 mV. In the absence of ISO, the 45Ca uptake in cells
preincubated in Na-free or 25 mM extracellular K (Ko) medium was
significantly greater than in cells preincubated in control medium. This
appeared to be due partly to increased 45Ca uptake via nifedipine-sensitive
pathways. These findings support the hypothesis that reduction in Nai
concentration ([Na]i) enhances the ISO-induced augmentation of Ca uptake
via nifedipine-sensitive pathways (presumably via slow Ca channels),
probably by a direct effect on the channels.
