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Department of Pediatrics, University of California, Los Angeles, School of Medicine, Harbor-UCLA Medical Center, Torrance, California 90509
In a variety of systemic blood vessels, protein kinase G (PKG)
plays a critical role in mediating relaxation induced by agents that
elevate cGMP, such as nitric oxide. The role of PKG in nitric oxide-
and cGMP-induced relaxation is less certain in the pulmonary circulation. In the present study, we examined the effects of inhibitors of PKG on the responses of isolated fourth-generation pulmonary veins of newborn lambs (10 ± 1 days of age) to nitric oxide and cGMP. In vessels preconstricted with endothelin-1, nitric oxide and 8-bromo-cGMP (a cell-membrane-permeable cGMP analog) induced
concentration-dependent relaxation. The relaxation was significantly
attenuated by
-phenyl-1,N2-etheno-8-bromoguanosine-3',5'-cyclic
monophosphorothionate (Rp-8-Br-PET-cGMPS; a PKG inhibitor) and
N-[2-(methylamino)ethyl]5-isoquinolinesulfonamide [H-8; an inhibitor of PKG and protein kinase A (PKA)] but
was not affected by KT-5720 (a PKA inhibitor). Biochemical study showed that PKG activity in newborn ovine pulmonary veins was inhibited by
8-Br-PET-cGMPS and H-8 but not by KT-5720. PKA activity was not
affected by 8-Br-PET-cGMPS but was inhibited by H-8 and KT-5720. These
results suggest that PKG is involved in relaxation of pulmonary veins
of newborn lambs induced by nitric oxide and cGMP.
guanosine 3',5'-cylic monophosphate; -phenyl-1,
N2-etheno-8-bromoguanosine
3',5'-monophosphorothioate; N-[2-(methylamino)ethyl]5-isoquinolinesulfonamide; KT-5720; vasodilation; neonatal pulmonary circulation
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