AJP - Cell Physiology, Vol 254, Issue 1 C75-C83, Copyright © 1988 by American Physiological Society
Ca dependence of Na influx during treatment of rabbit aorta with NE and high K solutions
P. I. Aaronson and A. W. Jones
Department of Pharmacology, St. George's Hospital Medical School, London, England.
Cellular influx of 24Na was measured in isolated rabbit aorta during
stimulation with 10 microM norepinephrine (NE) or depolarization with 80 mM
K solution, using a pulse-labeling, cold-wash technique. NE caused a two-
to threefold increase in Na influx; a smaller but significant increase was
also observed in depolarized tissues. Basal and NE-induced fluxes at 1 min
were significantly increased by a 20-min preincubation in a Ca-free
solution containing 2 mM EGTA; elevation of [Mg] in this solution reduced
these effects. The high K-induced influx was prevented by a combination of
low Ca (30 microns) and elevated Mg (10 mM). The Ca agonist, BAY-K 8644,
increased 24Na influx. The Ca antagonist, diltiazem, inhibited the
depolarization-stimulated 24Na influx in a concentration-dependent manner,
but was less effective in blocking the response to NE. Extension of the
preincubation in NE plus Ca-free medium from 30 s to 15 min decreased the
influx response and contraction. After exposure to NE in Ca-free solution,
24Na influx remained elevated 10 min after washing out NE in the continued
absence of Ca. A second exposure to NE at that time did not increase
influx. We propose that a component of 24Na influx during excitation
depends directly on a rise in intracellular [Ca]. The role of an indirect
effect of [Ca] on metabolic H+ production with subsequent stimulation of
the Na+-H+ exchange may also be a factor.
