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Am J Physiol Heart Circ Physiol 276: H1877-H1883, 1999;
0363-6135/99 $5.00
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Vol. 276, Issue 6, H1877-H1883, June 1999

5-(N-ethylcarboxamido)adenosine desensitizes the A2b-adenosine receptor in lung circulation

Johnson Haynes Jr., Boniface Obiako, Pavel Babal, and Troy Stevens

Pulmonary and Critical Care Division, Departments of Medicine, Physiology, Pathology, and Pharmacology, University of South Alabama College of Medicine, Mobile, Alabama 36688

The adenosine agonist 5-(N-ethylcarboxamido)adenosine (NECA) induces vasodilation in the pulmonary circulation via A2-adenosine-receptor activation. We addressed whether prolonged treatment with NECA desensitizes in A2-adenosine- receptor function in isolated lung and pulmonary artery smooth muscle cells (PASMC). In lung microcirculation preconstricted with a hypoxic gas, initial administration of NECA caused a 57% vasodilatory response after 3-4 min. Readministration of NECA after 45 min resulted in minimal vasodilation. The highest accumulation of PASMC cAMP occurred 3-5 min after NECA, coincident with NECA-induced vasodilation. In PASMCs treated with NECA for 45 min, cAMP did not increase. Isoproterenol- and indolidan-induced vasodilation remained intact in NECA-desensitized lungs. In NECA-desensitized PASMCs, isoproterenol-induced cAMP accumulation was decreased, suggesting a common mechanism of desensitization. cAMP accumulation was decreased in cholera toxin-treated NECA-desensitized PASMCs compared with cholera toxin-treated control PASMCs, demonstrating that Gsalpha -adenylyl cyclase signaling contributes to desensitization. The A2a-adenosine-receptor agonist CGS-21680C neither increased cAMP accumulation in PASMCs nor attenuated NECA-induced vasodilation. These data support that the A2b-adenosine receptor is responsible for pulmonary vasodilation and desensitization through mechanisms(s) involving Gsalpha -adenylyl cyclase signaling.

Gsalpha -adenylyl cyclase signaling; adenosine 3',5'-cyclic monophosphate; pulmonary artery vasodilation


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