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J Appl Physiol 84: 1535-1539, 1998;
8750-7587/98 $5.00
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Vol. 84, Issue 5, 1535-1539, May 1998

Developmental change in isoproterenol-mediated relaxation of pulmonary veins of fetal and newborn lambs

Yuansheng Gao, Jean-Francois Tolsa, Michael Botello, and J. Usha Raj

Department of Pediatrics, Harbor-UCLA Medical Center, University of California, Los Angeles, School of Medicine, Torrance, California 90509

beta -Adrenergic agonists are important regulators of perinatal pulmonary circulation. They cause vasodilation primarily via the adenyl cyclase-adenosine 3',5'-cyclic monophosphate (cAMP) pathway. We examined the responses of isolated fourth-generation pulmonary veins of term fetal (145 ± 2 days gestation) and newborn (10 ± 1 days) lambs to isoproterenol, a beta -adrenergic agonist. In vessels preconstricted with U-46619 (a thromboxane A2 analog), isoproterenol induced greater relaxation in pulmonary veins of newborn lambs than in those of fetal lambs. The relaxation was eliminated by propranolol, a beta -adrenergic antagonist. Forskolin, an activator of adenyl cyclase, also caused greater relaxation of veins of newborn than those of fetal lambs. 8-Bromoadenosine 3',5'-cyclic monophosphate, a cell membrane-permeable analog of cAMP, induced a similar relaxation of all vessels. Biochemical studies show that isoproterenol and forskolin induced a greater increase in cAMP content and in adenyl cyclase activity of pulmonary veins in the newborn than in the fetal lamb. These results demonstrate that beta -adrenergic-agonist-mediated relaxation of pulmonary veins increases with maturation. An increase in the activity of adenyl cyclase may contribute to the change.

beta -adrenergic agonist; adenyl cyclase; vascular smooth muscle; neonatal pulmonary circulation


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