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68 (3), NO Y ARTERIAS PULMONARES

modula la acción vasodilatadora del NO, siendo la NAD(P)H oxidasa de la
adventicia la principal fuente endógena del anión superóxido. La vasodilata-
ción inducida por el NO de origen endotelial y por el NO exógeno aumenta
con la edad, posiblemente por un incremento en la actividad de la ciclooxige-
nasa-1 en los primeros momentos de vida extrauterina que modularía el efec-
to vasodilatador del NO. Finalmente, encontramos que el NO y los donadores
de NO, SNAP y nitroprusiato (SNP), difieren en la cinética y distribución
regional de la liberación del NO, lo que influye en la susceptibilidad para la
inactivación por el anión superóxido y por la oxihemoglobina.

Palabras clave: Óxido nítrico, neonato, arterias pulmonares, superóxido.

SUMMARY

Nitric oxide- and nitric oxide donor-induced responses in piglet
pulmonary arteries: Postnatal maturation and modulation by oxidative
stress

We have analyzed the influence of postnatal age and oxidative stress
on the in vitro pulmonary vasodilator activity of nitric oxide and nitric oxide
donors. Isolated pulmonary arteries from 1 d and 2 week old piglets were
mounted for isometric force recording. Basal oxidative stress modulated the
vasodilator activity of nitric oxide, being the adventitial NADPH oxidase the
main endogenous source of superoxide anion. Endogenous and exogenous
NO-induced vasodilatation increased with age, possibly through an increased
cyclooxigenase-1 activity during the first hours of extrauterine life which
could inactivate NO. Finally, we found that NO and the NO donors SNP and
SNAP not only showed different kinetics and regional distribution of NO
release but also a different susceptibility to be inactivated by superoxide and
oxyhemoglobin.
Keywords: Nitric oxide, newborn, pulmonary arteries, superoxide

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