Journal
JOURNAL OF CARDIOVASCULAR PHARMACOLOGY
Volume 56, Issue 2, Pages 184-189Publisher
LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1097/FJC.0b013e3181e74d6a
Keywords
potassium channels; sepsis; tetraethylammonium; glibenclamide; apamin; iberiotoxin; vascular hyporesponsiveness
Funding
- Fundacao de Apoio a Pesquisa Cientifico e Tecnologica do Estado de Santa Catarina
- Conselho Nacional de Desenvolvimento Cietifico e Tecnologico
- Coordenacao de Aperfeicoamento de Pessoal de Nivel Superior (Brazil)
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This study investigated the involvement of potassium channel subtypes in the hyporesponsiveness to vasoconstrictors of an experimental model of sepsis [ cecal ligation and puncture (CLP)], at 2 time points, namely, 6 and 24 hours after sepsis onset. Wistar rats were submitted to CLP or sham surgery, and 6 and 24 hours later, responses to phenylephrine were obtained before and 30 minutes after injection of potassium channel blockers. The potassium channel blockers used were tetraethylammonium (TEA; a nonselective channel blocker), glibenclamide (GLB; an adenosine triphosphate -dependent channel blocker), 4-aminopyridine (4-AP; a voltage-dependent channel blocker), apamin (APA; a small-conductance calcium-dependent channel blocker), and iberiotoxin (IBTX; a large-conductance calciumdependent channel blocker). It was found that (1) sepsis caused a severe vascular hyporesponsiveness to phenylephrine both 6 and 24 hours after CLP, (2) TEA partially reversed the hyporesponsiveness 6 hours after CLP and completely restored vascular response to phenylephrine 24 hours after CLP, (3) apamin reversed hyporesponsiveness 6 but not 24 hours after CLP, (4) GLB restored phenylephrine response only 24 hours after CLP, and (5) IBTX and 4-AP were ineffective in all periods studied. Our results suggest that potassium channels are important effectors of sepsis-induced vascular dysfunction in vivo and that different subtypes of potassium channels are involved in early (smallconductance calcium-dependent potassium channels) and late (adenosine triphosphate -dependent potassium channels) hyporesponsiveness to vasoconstrictors caused by sepsis.
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