TY - JOUR
T1 - Role of potassium channels in regulation of brain arteriolar tone I
T2 - Comparison of cerebrum versus brain stem
AU - Horiuchi, Tetsuyoshi
AU - Dietrich, Hans H.
AU - Tsugane, Shinichiro
AU - Dacey, Ralph G.
PY - 2001
Y1 - 2001
N2 - Background and Purpose - 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 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. Results - Cerebral and brain stem arterioles were significantly constricted by 4-aminopyridine and low concentration of BaCl2 but not by glibenclamide. The addition of Nω-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 Nω-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.
AB - Background and Purpose - 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 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. Results - Cerebral and brain stem arterioles were significantly constricted by 4-aminopyridine and low concentration of BaCl2 but not by glibenclamide. The addition of Nω-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 Nω-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.
KW - arterioles
KW - brain stem
KW - microcirculation
KW - potassium channels
KW - rats
UR - http://www.scopus.com/inward/record.url?scp=0035148369&partnerID=8YFLogxK
U2 - 10.1161/01.STR.32.1.218
DO - 10.1161/01.STR.32.1.218
M3 - Article
C2 - 11136940
AN - SCOPUS:0035148369
VL - 32
SP - 218
EP - 224
JO - Stroke
JF - Stroke
SN - 0039-2499
IS - 1
ER -