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Department of Physiology, University of Utah School of Medicine, Salt Lake City, Utah 84108
Received 30 October 1996; accepted in final form 7 February 1997.
Chen, J., B. Dinger, and S. J. Fidone. cAMP production
in rabbit carotid body: role of adenosine. J. Appl.
Physiol. 82(6): 1771-1775, 1997.
In the present
study, we have investigated the possible role of adenosine in the
hypoxia-mediated increase in adenosine 3
,5
-cyclic
monophosphate (cAMP) in the carotid body. cAMP levels in rabbit carotid
bodies superfused in vitro for 10 min were increased in the presence of
adenosine (100 µM and 1.0 mM; maximum increase = 127%,
P < 0.01). These effects were
reduced by the nonspecific adenosine-receptor antagonist 1,3-dipropyl-8[p-sulfophenyl]xanthine
(DPSPX; 10 µM). The specific A2-receptor agonist
2-[4
(2-carboxymethyl)phenylethylamino]-5
-N-ethylcarboxamido adenosine (CGS-21680; 100 nM) also elevated carotid body cAMP levels,
an effect that was blocked by the specific
A2-antagonist 3,7-dimethyl-L-propargyl-xanthine
(DMPX; 50 µM). Hypoxia-evoked elevations in cAMP were potentiated in
the presence of the adenosine-uptake inhibitor dipyridamole (100 nM)
and blocked by exposure to adenosine-receptor antagonists. Our data
suggest that the rabbit carotid body contains specific adenosine
receptors (A2 subtype) that are
positively coupled to adenylate cyclase and that increases in cAMP
associated with hypoxia are mediated by the release of endogenous
adenosine.
hypoxia; adenylate cyclase; chemoreception; chemotransduction
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