What does this research mean for the field?

The rapidly activating delayed-rectifying K+ current (I(Kr)) in guinea-pig ventricular myocytes is not acutely regulated by protein tyrosine kinases (PTK) or phosphotyrosyl phosphatases (PTP). Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

May 22, 2006British Journal of PharmacologyOpen Access

Insensitivity of cardiac delayed‐rectifier IKr to tyrosine phosphorylation inhibitors and stimulators

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Structured PICO

Population

Guinea-pig ventricular myocytes configured for ruptured-patch or perforated-patch voltage-clamp

Intervention

Protein tyrosine kinase (PTK) inhibitors (tyrphostin A23, tyrphostin A25, genistein) and promoters of tyrosine phosphorylation (orthovanadate, exogenous c-Src PTK, insulin, IGF-1, EGF, bFGF)

Comparator

PTK-inactive analogues (tyrphostin A1, daidzein) or untreated baseline

Outcome

Amplitude of I(Kr) tail currentsurrogate

The rapidly activating delayed-rectifying K+ current (I(Kr)) in guinea-pig ventricular myocytes is not acutely regulated by tyrosine phosphorylation.

Authors

SMSergey MissanDalhousie University PZPavel ZhabyeyevUniversity of Alberta PLPaul LinsdellDalhousie University

Discussion

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Implication

Guinea-pig data indicate no acute PTK regulation of I(Kr); leaves open species-specific or chronic effects in human electrophysiology.

Cite This Study

Missan et al. (2006) studied this question.

synapsesocial.com/papers/6a1e01fb348274ea529fbe64 https://doi.org/10.1038/sj.bjp.0706776

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