Role of potassium channels in regulation of brain arteriolar tone: comparison of cerebrum versus brain stem.
OBJECTIVE
Potassium 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.


METHODS
Penetrating cerebral (40. 9+/-2.2 microm control diameter) and brain stem (36.2+/-1.2 microm) 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.


RESULTS
Cerebral and brain stem arterioles were significantly constricted by 4-aminopyridine and low concentration of BaCl(2) but not by glibenclamide. The addition of N:(omega)-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:(omega)-nitro-L-arginine.


CONCLUSIONS
Voltage-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.
Horiuchi
T
T
Department of Neurosurgery, Washington University School of Medicine, St Louis, MO 63110, USA.
Dietrich
H H
HH
Tsugane
S
S
Dacey
R G
RG
D015761:4-Aminopyridine / Q000494:pharmacology; D000818:Animals; D001160:Arterioles / Q000187:drug effects / Q000378:metabolism*; D017609:Barium Compounds / Q000494:pharmacology; D001921:Brain / Q000098:blood supply / Q000378:metabolism*; D001933:Brain Stem / Q000098:blood supply / Q000378:metabolism; D002712:Chlorides / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005905:Glyburide / Q000494:pharmacology; D006863:Hydrogen-Ion Concentration; D066298:In Vitro Techniques; D008297:Male; D019001:Nitric Oxide Synthase / Q000037:antagonists & inhibitors; D019335:Nitroarginine / Q000494:pharmacology; D020110:Pinacidil / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism / Q000494:pharmacology; D026902:Potassium Channel Blockers; D015221:Potassium Channels / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013687:Telencephalon / Q000098:blood supply / Q000378:metabolism; D019789:Tetraethylammonium / Q000494:pharmacology; D014661:Vasoconstriction / Q000187:drug effects / Q000502:physiology*; D014665:Vasodilator Agents / Q000494:pharmacology
D017609:Barium Compounds; D002712:Chlorides; D004791:Enzyme Inhibitors; D026902:Potassium Channel Blockers; D015221:Potassium Channels; D014665:Vasodilator Agents; C024986:barium chloride; D019335:Nitroarginine; D019789:Tetraethylammonium; D020110:Pinacidil; D015761:4-Aminopyridine; D019001:Nitric Oxide Synthase; D011188:Potassium; D005905:Glyburide