Referenced in: none

Automatically associated channels: Kir2.3

Title: Oxygen dilation in fetal pulmonary arterioles: role of K(+) channels.

Authors: J R Gosche

Journal, date & volume: J. Surg. Res., 2001 May 15 , 97, 159-63

PubMed link: http://www.ncbi.nlm.nih.gov/pubmed/11341793

Abstract
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.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) <or=50 mm Hg). 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.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.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.