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upon the Newborn Rat Pulmonary Arterial Muscle and Endothelium
1 Department of Pediatrics, University of Toronto, Toronto, Ontario, Canada
2 Department of Pediatrics, University of Toronto, Toronto, Ontario, Canada; Department of Physiology, University of Toronto, Toronto, Ontario, Canada
3 Department of Pharmacology, University of Toronto, Toronto, Ontario, Canada
* To whom correspondence should be addressed. E-mail: Jaques.Belik{at}sickkids.ca.
8-iso-Prostaglandin F2
(8-iso-PGF2) is a bioactive lipid peroxidation product that is a vasoconstrictor at high concentrations. Paradoxically, at lower, and possibly physiologic concentrations is a pulmonary vascular muscle relaxant. Its effects on newborn pulmonary vasculature are unknown. We hypothesized that the pulmonary arterial 8-iso-PGF2 responses may be developmentally regulated. Therefore, the purpose of this study was to evaluate and compare 8-iso-PGF2 effects between one- and two-week-old newborn and adult rat isolated intrapulmonary arteries (100 µm) mounted on a myograph. Force following 8-iso-PGF2 stimulation was greatest in the adult (P<0.01). In newborns, force was significantly increased by the nitric oxide (NO) synthase inhibitor, LNAME (P<0.01) and was suppressed by blockade of the thromboxane (TX) A2 receptor. Whereas 8-iso-PGF2 induced a significant dose-dependent relaxation of adult pre-contracted vessels in the presence of a TXA2 -mimetic (U46619 1 µM), contraction was observed in the one-week-old rat. This 8-iso-PGF2-induced contraction was abolished by endothelium removal and LNAME, and attenuated by the cyclooxygenase inhibitor, ibuprofen. In the presence of a TP receptor blocker, 8-iso-PGF2 induced NO-mediated relaxation the magnitude of which was greater in the newborn, as compared to the adult (P<0.01). When exposed to 8-iso-PGF2 in vitro, only the newborn lung secreted TXB2. We conclude that, in contrast to its relaxant effect in the adult, 8-iso-PGF2 induces contraction of the pulmonary arteries in the early postnatal period, which is likely to be mediated by endothelium-derived TXA2. This phenomenon may contribute to the maintenance of a higher pulmonary vascular resistance in the early postnatal period.
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