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Am J Physiol Heart Circ Physiol 280: H83-H89, 2001;
0363-6135/01 $5.00
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Vol. 280, Issue 1, H83-H89, January 2001

Adenosine A2A receptors mediate cardiovascular responses to hypoxia in fetal sheep

Brian J. Koos and Takatsugu Maeda

Nicholas S. Assali Perinatal Research Laboratory, Departments of Obstetrics and Gynecology, Brain Research Institute, University of California at Los Angeles School of Medicine, Los Angeles, California 90095-1740

Nonselective adenosine (ADO) receptor antagonists block hypoxia-induced bradycardia and hypertension in fetal sheep. This study was designed to determine the ADO receptor subtype that is involved in these cardiovascular responses. In chronically catheterized fetal sheep (>0.8 term), fetal hypoxemia was induced by having the ewe breathe a hypoxic gas mixture (9% O2-3% CO2-88% N2) for 1 h. Intra-arterial infusion of ZM-241385, an antagonist highly selective for ADO A2A receptors, to eight fetuses during normoxia significantly increased mean arterial pressure (MAP) from 42.5 ± 2.0 to 46.1 ± 2.0 mmHg without altering heart rate (HR). Infusion of a selective antagonist of ADO A1 receptors [1,3-dipropyl-8-cyclopentylxanthine (DPCPX)] elevated MAP and HR only after the infusion was terminated, although administration of the vehicle for ZM-241385 or DPCPX had no effect on MAP or HR. Isocapnic hypoxia with infusion of DPCPX or the vehicle for DPCPX or ZM-241385 produced a transient fall in HR, a rise in MAP, and a decrease in plasma volume. In contrast, ADO A2A receptor blockade abolished the hypoxia-induced bradycardia and hypertension and blunted the decline in plasma volume. We conclude that fetal ADO A2A receptors: 1) modulate AP during normoxia, and 2) mediate cardiovascular responses during acute O2 deficiency.

arterial pressure; autonomic nervous system; blood flow; fetus; heart rate


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