| 11341793 |
Gosche JR: Oxygen dilation in fetal pulmonary arterioles: role of K (+) channels. J Surg Res. 2001 May 15;97(2):159-63.
BACKGROUND: Oxygen is a potent stimulus for pulmonary vasodilation. Potassium channels have been implicated as both sensors and effectors for oxygen-induced changes in pulmonary vascular tone. We have examined the effect of potassium channel blockers on oxygen-induced vasodilation in isolated pulmonary arterioles from fetal rats at term. MATERIALS and METHODS: Third generation pulmonary arterioles were isolated from fetal rats on Day 22 of gestation, cannulated, pressurized at constant distending pressures, and preconstricted by suffusion with a salt solution bubbled with a "hypoxic gas" mixture (pO (2) Oxygen-induced vasodilation was measured as percentage reversal of the "hypoxic" vasoconstriction after 30 min of suffusion with "normoxic" solution (pO (2) 90-145 mm Hg). Responses were recorded in the absence of blockers (controls) or in the presence of a voltage-gated K (+) channel (K (v)) blocker, 4-aminopyridine; an ATP-sensitive K (+) channel (K (ATP)) blocker, glibenclamide; a Ca (2+)-activated K (+) channel (K (Ca)) blocker, charybdotoxin; or a nonspecific K (+) channel blocker, tetraethylammonium. RESULTS: In control arterioles, normoxic suffusion for 30 min reversed hypoxic preconstriction by 83 +/- 19%. 4-aminopyridine significantly attenuated (44 +/- 9%), and glibenclamide and charybdotoxin had no effect (80 +/- 16 and 79 +/- 20%) on the magnitude of normoxic vasodilation. CONCLUSIONS: Our results are consistent with a contribution of K (v) channels, but not K (ATP) or K (Ca) channels, to oxygen-induced vasodilation in third generation pulmonary arterioles from term fetal rats. |
1(0,0,0,1) |