Journal of Applied Physiology, Vol 62, Issue 6 2246-2251, Copyright © 1987 by American Physiological Society
Platelet aggregation increases cholinergic neurotransmission in canine airway
J. Tamaoki, K. Sekizawa, M. L. Osborne, I. F. Ueki, P. D. Graf and J. A. Nadel
To determine whether thromboxane A2 released from aggregating platelets
increases the contractile response of airway smooth muscle to cholinergic
nerve stimulation and, if so, what the mechanism of action is, we studied
in vitro bronchial segments from dogs under isometric conditions. The
contractile responses to electrical field stimulation at 30 s and 1 min
after the addition of autologous platelets were increased by 11.1 +/- 3.2
(SD) and 20.7 +/- 5.4%, respectively, and were accompanied by the release
of thromboxane A2. These effects were inhibited either by pretreatment of
platelets with indomethacin or by addition of the thromboxane A2 receptor
antagonist SQ 29548. Likewise, the thromboxane A2 mimetic U 46619, in
subthreshold doses (i.e., insufficient to increase base-line tension),
increased electrical field stimulation-induced contraction by 18.7 +/-
4.8%. The increase was greater in the presence of a concentration of
physostigmine that did not cause spontaneous contraction and was blocked by
SQ 29548 but not by hexamethonium or by phentolamine. Methacholine-induced
contractions were unaffected by U 46619. These results indicate that
aggregating platelets, by releasing thromboxane A2, increase the airway
contractile response to neural stimulation probably by the accelerated
release of acetylcholine.
