Open AccessVasodilation Mediated by Inward Rectifier K+ Channels in Cerebral Microvessels of Hypertensive and Normotensive Rats
Author(s) -
Katsutoshi Nakahata,
Hiroyuki Kinoshita,
Yasuyuki Tokinaga,
Yuko Ishida,
Yoshiki Kimoto,
Mayuko Dojo,
Kazuhiro Mizumoto,
Koji Ogawa,
Yoshio Hatano
Publication year - 2006
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/01.ane.0000194303.00844.5e
Subject(s) - vasodilation , medicine , inward rectifier potassium ion channel , arteriole , microcirculation , cerebral arteries , endocrinology , potassium channel , sodium nitroprusside , anesthesia , nitric oxide , ion channel , receptor
Although inward rectifier K+ channels contribute to the regulation of cerebral circulation, dilation of cerebral microvasculature mediated by these channels has not been demonstrated in chronic hypertension. We designed the present study to examine the roles of inward rectifier K+ channels in the vasodilation produced by increased levels of extracellular K+ in cerebral parenchymal arterioles from hypertensive and normotensive rats. During constriction to prostaglandin F2alpha (5 x 10(-7) M), the arterioles within brain slices were evaluated using computer-assisted microscopy. Potassium chloride (KCl) induced vasodilation in cerebral arterioles from normotensive (5-10 mM) and hypertensive (5-15 mM) rats, whereas an inward rectifier K+ channel antagonist barium chloride (BaCl2; 10(-5) M) completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rats. In contrast, the vasodilator responses induced by sodium nitroprusside (3 x 10(-8) to 3 x 10(-6) M) in these two strains were similar. These results suggest that in cerebral cortex parenchymal microvessels, inward rectifier K+ channels play a crucial role in vasodilation produced by extracellular K+ and that the dilation of cerebral arterioles via these channels is augmented in chronic hypertension.