(Stroke. 2001;32:218.)
© 2001 American Heart Association, Inc.
Original Contributions |
From the Department of Neurosurgery, Washington University School of Medicine, St Louis, Mo.
Correspondence to Hans H. Dietrich, PhD, Department of Neurosurgery, Washington University School of Medicine, Box 8057, 660 S Euclid Ave, St Louis, MO 63110. E-mail dietrich_h{at}kids.wustl.edu
Background and PurposePotassium channels are important regulators of resting tone in large cerebral arteries, but their activity and distribution may vary according to vessel location and species studied. In the cerebral microcirculation in vivo, however, these channels appear to be silent at rest. Our goal was to determine the activity of potassium channels of brain arterioles from 2 origins under basal conditions in vitro.
MethodsPenetrating cerebral (40.9±2.2 µm control diameter) and brain stem (36.2±1.2 µm) arterioles of rats were prepared from middle cerebral and basilar arteries, respectively. The internal diameter of cannulated and pressurized vessel was monitored with the inverted microscope before and after administration of potassium channel inhibitors. In addition, we studied the effect of nitric oxide synthase inhibition on potassium channel activity.
ResultsCerebral
and brain stem arterioles were significantly constricted by
4-aminopyridine and low concentration of
BaCl2 but not by glibenclamide. The addition of
N
-nitro-L-arginine
to 4-aminopyridine further decreased diameters of both
arterioles. Tetraethylammonium ion caused a
significant constriction of brain stem but not cerebral arteriole. The
brain stem arteriole was further constricted by additional
N
-nitro-L-arginine.
ConclusionsVoltage-dependent and inward-rectifier, but not ATP-sensitive, potassium channels are active under basal conditions of rat cerebral and brain stem arterioles. There is a regional difference in the activity of calcium-activated potassium channels, which, at rest, are open in brain stem but silent in cerebral arterioles. In addition, basal endogenous nitric oxide may not contribute to the activation of voltage-dependent and calcium-activated potassium channels.
Department of Internal Medicine, Cardiovascular Division, University of Iowa College of Medicine, Iowa City, Iowa
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