Meanings of activate potassium in inglês

Calcium- activated potassium channels mediate many biologically important functions in electrically excitable cells.

High-conductance calcium- activated potassium (maxi-K) channels comprise a specialized family of K+ channels.

Objective: Adenosine dilates human coronary arteries by activating potassium channels in an endothelial cell-independent manner.

Calcium- and voltage- activated potassium channels (BK) are regulated by a multiplicity of signals.

Small conductance calcium- activated potassium (SK) channels provide protection in different paradigms of neuronal cell death.

Calcium- activated potassium (K(Ca)) channels are present throughout the central nervous system as well as many peripheral tissues.

We looked at the response of ion channel blockers directed at sodium, voltage-dependent calcium and ATP- activated potassium ion channels.

Neuronal calcium- activated potassium channels of the BK type are activated by membrane depolarization and intracellular Ca(2+) ions.

Voltage-dependent calcium channel blockers had little effect on the initiation or propagation of the spread, as did the ATP- activated potassium channel blocker.

The present study is to explore the role of large conductance calcium- activated potassium channels (BK Ca) in stretch-induced relaxation of colon.

Studies on voltage- activated potassium (Kv) channels show that voltage-sensor activation is sensitive to the composition of lipids in the surrounding membrane.

Large-conductance calcium- and voltage- activated potassium (BK) channels play a fundamental role in the signaling pathways regulating mouse anterior pituitary corticotrope function.

Small conductance (SK) calcium- activated potassium channels are found in many tissues throughout the body and open in response to elevations in intracellular calcium.

Amphipathic protein toxins from tarantula venom inhibit voltage- activated potassium (Kv) channels by binding to a critical helix-turn-helix motif termed the voltage sensor paddle.

Alternative exon splicing and reversible protein phosphorylation of large conductance calcium- activated potassium (BK) channels represent fundamental control mechanisms for the regulation of cellular excitability.

Voltage- activated potassium (Kv) channels open to conduct K+ ions in response to membrane depolarization, and subsequently enter non-conducting states through distinct mechanisms of inactivation.