Role of Na(+)-K(+)-ATPase in sodium nitroprusside-induced relaxation of pulmonary artery under hypoxia.
BACKGROUND
The sodium pump (Na(+)-K(+)-ATPase) plays a part in the regulation of smooth muscle contractility, and alterations of enzyme activity by hypoxia could contribute to the mechanism of hypoxic pulmonary vasoconstriction.


OBJECTIVE
To determine the role of Na(+)-K(+)-ATPase in the sodium nitroprusside (SNP)-induced relaxation of pulmonary artery in hypoxia.


METHODS
Using isolated canine pulmonary arterial rings, we measured the relaxant responses of KCI-contracted tissues to SNP under hyperoxic (95% O2, 5% O2) and hypoxic conditions (5% O2, 5% CO2, 90% N2 in vitro. Na(+)-K(+)-ATPase activity was assessed by measuring ouabain-sensitive (86)Rb uptake.


RESULTS
The SNP-induced relaxation was reduced under hypoxia, so that the maximal relaxation decreased from 80.1 +/- 8.6 to 57.8 +/- 6.8% (p < 0.01) and the concentration of SNP required to produce 50% relaxation increased from 1.9 +/- 0.4 x 10(-6) to 2.6 +/- 0.6 x 10(-5) M (p < 0.01). Addition of ouabain, an Na(+)-K(+)-ATPase inhibitor, attenuated the relaxant response to SNP and this inhibition was still observed under hypoxia. Incubation of endothelium-denuded rings with SNP caused dose-dependent increases in intracellular cGMP levels and ouabain-sensitive (86)Rb uptake, and these effects were not significantly altered by hypoxia.


CONCLUSIONS
These results suggest that sarcolemmal Na(+)-K(+)-ATPase activity may be implicated in the mechanism of nitrovasodilator-induced vasodilation of pulmonary artery and may still be functioning under hypoxia.
Tagaya
E
E
First Department of Medicine, Tokyo Women's Medical University School of Medicine, Tokyo, Japan.
Tamaoki
J
J
Kawatani
K
K
Nagai
A
A
D000818:Animals; D004285:Dogs; D005260:Female; D000860:Hypoxia / Q000503:physiopathology*; D066298:In Vitro Techniques; D008297:Male; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000502:physiology*; D009599:Nitroprusside / Q000494:pharmacology; D011651:Pulmonary Artery / Q000502:physiology*; D000254:Sodium-Potassium-Exchanging ATPase / Q000502:physiology*; D014664:Vasodilation / Q000187:drug effects / Q000502:physiology*
D009599:Nitroprusside; D000254:Sodium-Potassium-Exchanging ATPase