Effect of adenosine on adrenergic neurotransmission and modulation
by endothelium in canine pulmonary artery.
Tamaoki, Jun, Etsuko Tagaya, Atsushi Chiyotani, Hisashi Takemura,
Atsushi Nagai, Kimio Konno, Takamasa Onuki, and Sumio Nitta.
First Department of Medicine and Department of Thoracic Surgery,
Tokyo Women's Medical College, Tokyo 162, Japan
APStracts 3:0508H, 1996.
To determine the effect of adenosine on adrenergic neurotransmission
in pulmonary vasculature and its modulation by endothelial cells, we
studied canine pulmonary arteries under isometric conditions in
vitro. Adenosine decreased the contractile responses to electrical
field stimulation, but was without effect on those to noradrenaline.
This inhibitory effect was concentration-dependent, with the rank
order of potency being 5'-(N-ethylcarboxamido) adenosine (NECA)
> 2-chloroadenosine > adenosine >> N6-2
-(4-aminophenyl) ethyl adenosine (APNEA), an A3 adenosine receptor
agonist > CGS 21680, an A2a agonist > 2-chloro-N6
-cyclopentyladenosine (CCPA), an A1 agonist. Adenosine reduced the
electrical field stimulation-evoked 3H-overflow in superfused
pulmonary artery previously soaked in 3H-noradrenaline. Pretreatment
with the adenosine uptake blocker dipyridamole or the adenosine
deaminase inhibitor deoxycoformycin enhanced the adenosine action,
and this enhancement was not observed in the endothelium-denuded
tissues. Adenosine deaminase activity was found in endothelial cells.
Therefore, adenosine inhibits noradrenaline release via A2b receptor
mechanism, an effect that may be modulated by uptake and metabolism
by endothelial cells.
Received 18 July 1996; accepted in final form 9 October 1996.
APS Manuscript Number H641-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996