Format

Send to:

Choose Destination
See comment in PubMed Commons below
Anesth Analg. 2006 Feb;102(2):571-6.

Vasodilation mediated by inward rectifier K+ channels in cerebral microvessels of hypertensive and normotensive rats.

Author information

  • 1Department of Anesthesiology, Wakayama Medical University, Wakayama, Japan.

Abstract

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.

PMID:
16428563
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Lippincott Williams & Wilkins
    Loading ...
    Write to the Help Desk