Blockade of Vascular Potassium Channels During Human Endotoxemia

2014-08-27 03:50:19 | BioPortfolio


Background: Activation of NO-synthase and vascular potassium (K) channels may play a role in the sepsis-induced attenuated sensitivity to norepinephrine. We examined whether various K channel blockers and NO-synthase inhibition could restore norepinephrine sensitivity during experimental human endotoxemia.

Study Design

Allocation: Randomized, Control: Active Control, Endpoint Classification: Pharmacokinetics/Dynamics Study, Intervention Model: Parallel Assignment, Masking: Open Label, Primary Purpose: Treatment




endotoxin, Potassium channel blockers: TEA, Quinin, Tolbutamide, L-NMMA




Radboud University

Results (where available)

View Results


Published on BioPortfolio: 2014-08-27T03:50:19-0400

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Medical and Biotech [MESH] Definitions

One of the POTASSIUM CHANNEL BLOCKERS, with secondary effect on calcium currents, which is used mainly as a research tool and to characterize channel subtypes.

A class of drugs that act by inhibition of potassium efflux through cell membranes. Blockade of potassium channels prolongs the duration of ACTION POTENTIALS. They are used as ANTI-ARRHYTHMIA AGENTS and VASODILATOR AGENTS.

A very slow opening and closing voltage-gated potassium channel that is expressed in NEURONS and is closely related to KCNQ2 POTASSIUM CHANNEL. It is commonly mutated in BENIGN FAMILIAL NEONATAL CONVULSIONS.

A delayed rectifier subtype of shaker potassium channels that is the predominant VOLTAGE-GATED POTASSIUM CHANNEL of T-LYMPHOCYTES.

A voltage-gated potassium channel that is expressed primarily in the HEART.

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