Abstract
In vivo exposure to hyperoxic environment modifies the in vitro vasomotor response of pulmonary and systemic vessels. We hypothesized that prenatal exposure to hyperoxia would alter the development of ductus arteriosus (DA) reactivity. Hyperoxia was induced by incubating fertilized eggs at 60% O2 from day 15 to 19 of the 21‐d incubation period. DA contractility was studied on day 19 (non‐internally‐pipped embryos) Relaxant responses were studied after precontraction with 125 mM KCl. Hyperoxia did not affect embryonic survival or growth. The contractions induced by 21% O2, KCl, the inhibitor of KV channels 4‐aminopyridine, phenylephrine, and endothelin‐1 and the relaxations induced by acetylcholine, sodium nitroprusside, forskolin, isoproterenol, and the Rho kinase inhibitor OH‐fasudil were similar in DA from embryos incubated under normoxic or hyperoxic conditions. In contrast, the membrane permeable hydroperoxide t‐butyl‐hydroperoxide (1 μM–0.1mM) induced concentration‐dependent contraction in the DA from normoxic embryos and relaxation in the DA from hyperoxic embryos. Reactive oxygen species are complex signalling molecule that produce relaxation in some vessels and contraction in others. Our results indicate that exposure to oxidant stress is capable of modifying the pattern of response of the DA to hydrogen peroxide.Supported by “Fundación de Investigación Médica Mutua Madrileña”
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