Role of na+i and ca2+i in nicotine-induced norepinephrine release
from bovine adrenal chromaffin cells.
Gerber, Stefan H., Armin Haunstetter, Carsten Kruger,
Alexander Kaufmann, Rainer Nobiling, and Markus Haass.
Departments of Cardiology and Experimental Surgery, University of
Heidelberg, Bergheimer Strae 58, D-69115 Heidelberg, Germany
APStracts 2:0131C, 1995.
The intracellular free sodium (Na+i) and calcium (Ca2+i)
concentrations were determined by SBFI and Fura-2 microfluorimetry,
respectively, in bovine adrenal chromaffin cells (BCC). Validation of
SBFI microfluorimetry by in vitro and in vivo calibration revealed a
reliable assessment of Na+i within a range of 1-30 mmol/l in single
BCC. Nicotine (0.1-10 [mu]mol/l) induced concentration-dependent
increases of both Na+i (from 3.3 +/- 0.1 to 25.6 +/- 0.4 mmol/l, n =
76, p < 0.001) and Ca2+i (from 64 +/- 1 to 467 +/- 16 nmol/l, n =
87, p < 0.001), which were accompanied by an increase of 3H
-norepinephrine release. Consistent with an exocytotic release
mechanism, nicotine-induced increments of Ca2+i and 3H-norepinephrine
release were reduced under calcium-free conditions and by gadolinium
chloride (40 [mu]mol/l), whereas Na+i was not affected. In contrast,
a parallel attenuation of nicotine-evoked changes in Na+i, Ca2+i and
3H-norepinephrine release was observed during reduction of the
extracellular sodium concentration (Na+o). The nicotine-evoked
responses was neutralized by the nicotinic receptor antagonist
hexamethonium (100 [mu]mol/l), but not by blockade of voltage
-dependent sodium channels (tetrodotoxin 1 [mu]mol/l). In conclusion,
the nicotine-induced exocytotic release of 3H-norepinephrine is
triggered by an increase of Ca2+i which is facilitated by sodium
influx through the nicotinic receptor ionophore.
Received 14 October 1994; accepted in final form 28 February
1995.
APS Manuscript Number C613-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 21 March 1995.