TY - JOUR
T1 - Platelet aggregation increases cholinergic neurotransmission in canine airway
AU - Tamaoki, J.
AU - Sekizawa, K.
AU - Osborne, M. L.
AU - Ueki, I. F.
AU - Graf, P. D.
AU - Nadel, J. A.
N1 - Funding Information:
From the Department of Medicine, Montreal Heart Institute and the University of Montreal Medical School, Montreal, Quebec, Canada. Thsi study was supported in part by grants from the Jean-Louis Levesque Foun dation and the Montreal Heart Institute Research Fund, Montreal, Quebec, Canada.
PY - 1987
Y1 - 1987
N2 - 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 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.
AB - 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 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.
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U2 - 10.1152/jappl.1987.62.6.2246
DO - 10.1152/jappl.1987.62.6.2246
M3 - Article
C2 - 3038826
AN - SCOPUS:0023183079
SN - 8750-7587
VL - 62
SP - 2246
EP - 2251
JO - Journal of Applied Physiology
JF - Journal of Applied Physiology
IS - 6
ER -