Modulation of hypoxic and acidic transduction cascades in the
rabbit carotid body by fluoride and cholera and pertussis toxins.
Cachero, T. G., A. Rocher, R. J. Rigual, and C. Gonzalez.
Departamento de Bioqu[acute]imica y Biolog[acute]ia Molecular y
Fisiolog[acute]ia, Facultad de Medicina. Universidad de Valladolid,
47005 Valladolid. -Spain-
APStracts 2:0217C, 1995.
The regulation of the chemoreceptor cell function by G proteins has
been studied by measuring the release of 3H-labelled catecholamine
(3H-CA) in carotid bodies (CB) treated with fluoride, cholera toxin
(CTX) and pertussis toxin (PTX). Fluoride augmented the basal release
of 3H-CA in a dose (5-20 mM) and Ca2+-dependent manner. Nisoldipine
(1 [mu]M) and ethylisopropylamiloride (EIPA;10 [mu]M) inhibited this
effect by nearly equal to 60%, and both drugs combined inhibited it
in full. Bay K 8644 (1 [mu]M) doubled the effect of fluoride. The
effects of fluoride on the stimulus-evoked release of 3H-CA varied
with the type of stimulus and the duration of the treatment.
Simultaneous application of fluoride with the stimulus increased by
five times the release evoked by hypoxia, and by two times that by K+
and DNP. Preincubation with fluoride for 1 h caused an inhibition (
nearly equal to 70%) of the release evoked by high K+ and
veratridine, while that evoked by DNP and low PO2 was still augmented
( nearly equal to x2). Preincubation (4 h) of the CBs with CTX (3
[mu]g/ml) reduced by 54% the release of 3H-CA evoked by 35 mM K+ but
did not affect that evoked by low PO2 or DNP. A similar treatment
with PTX (1 [mu]g/ml) affected only the release of 3H-CA evoked by
DNP, reducing it by 65%. The data show that fluoride, CTX and PTX
have different effects on the release of 3H-CA evoked by high
external K+, DNP and low PO2 indicating that the stimulus-secretion
coupling process for each stimulus is differently regulated by G
proteins.
Received 25 July 1994; accepted in final form 25 May 1995.
APS Manuscript Number C435-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 June 1995.