August 1, 1997Circulation Research

Endothelin-1 Inhibits the Slow Component of Cardiac Delayed Rectifier K+Currents via a Pertussis Toxin–Sensitive Mechanism

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Population

Ventricular myocytes enzymatically isolated from guinea pig hearts

Comparison

Endothelin-1 applied at nanomolar concentrations vs Basal conditions or isoproterenol-enhanced…

Design

Preclinical

Authors

TWTakashi WashizukaKyoto University MHMinoru HorieElectrophysiology MWMasato WatanukiHamamatsu Rosai Hospital

Discussion

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Implication

ET-1 suppression of enhanced IKs in animal myocytes is hypothesis-generating; leaves open effects on human repolarization or arrhythmogenesis.

Structured PICO

Population

Ventricular myocytes enzymatically isolated from guinea pig hearts

Intervention

Endothelin-1 (ET-1) applied at nanomolar concentrations

Comparator

Basal conditions or isoproterenol-enhanced conditions without ET-1

Outcome

Amplitude of the cardiac delayed rectifier K+ current (IK), specifically the slow component (IKs)surrogate

ET-1 inhibits the slow component of cardiac delayed rectifier K+ currents via an ETA receptor and PTX-sensitive G protein/PKA pathway, providing mechanistic insights into its electrophysiological effects.

Cite This Study

Washizuka et al. (1997) studied this question.

synapsesocial.com/papers/6a7299d3439bab0cabc3e192 https://doi.org/10.1161/01.res.81.2.211

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Implication

ET-1 suppression of enhanced IKs in animal myocytes is hypothesis-generating; leaves open effects on human repolarization or arrhythmogenesis.

Endothelin-1 Inhibits the Slow Component of Cardiac Delayed Rectifier K+Currents via a Pertussis Toxin–Sensitive Mechanism

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Endothelin-1 Inhibits the Slow Component of Cardiac Delayed Rectifier K+Currents via a Pertussis Toxin–Sensitive Mechanism

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider