What is the clinical evidence from this study?

Study design: Other. Intervention: dKv3.1 cloning and expression. Primary outcome: Molecular basis of IKur,d in dog atrium.

What question did this study set out to answer?

To identify the molecular basis of the ultrarapid delayed rectifier potassium current (IKur,d) in canine atrial myocytes and establish whether Shaw subfamily (Kv3) subunits are expressed in cardiac tissue.

September 1, 2000The Journal of PhysiologyOpen Access

Molecular evidence for a role of Shaw (Kv3) potassium channel subunits in potassium currents of dog atrium

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Key result

The Shaw-type channel dKv3.1 is present in dog atrium, but not ventricle, and is the likely molecular basis of canine atrial ultrarapid delayed rectifier current (IKur,d).

Population

Dog atrial myocytes, canine ventricular myocytes, and Xenopus oocytes

Design

Preclinical

Authors

LYLixia YueElectrophysiology ZWZhiguo WangON Semiconductor (United States)HRHansjörg RindtMissouri College

Discussion

Member takes

Implication

Enables molecular studies of atrial repolarization; leaves open human relevance and therapeutic potential.

Key Points

To identify the molecular basis of the ultrarapid delayed rectifier potassium current (IKur,d) in canine atrial myocytes and establish whether Shaw subfamily (Kv3) subunits are expressed in cardiac tissue.
Cloned a 1,755-bp full-length cDNA (dKv3.1) from canine atrium using homology-based RT-PCR and expressed it heterologously in Xenopus oocytes.
Characterized channel gating, kinetics, and pharmacological inhibition using extracellular 4-aminopyridine (4-AP) and tetraethylammonium (TEA).
Assessed transcript and protein expression across canine atrial and ventricular myocytes via RNase protection assays, Western blot, immunohistochemistry, and whole-cell patch-clamp recordings.
Cloned dKv3.1 exhibited 94.2% nucleotide and 99.3% amino acid homology to rat brain Kv3.1, reproducing native atrial IKur,d voltage dependence, kinetics, and sensitivity to 4-AP and TEA when expressed in oocytes.
Canine atrium selectively expressed the Kv3.1b splice variant transcript and protein, whereas the alternative candidate Kv1.5 was absent.
Whole-cell patch clamping, Western blots, and immunohistochemistry showed that both IKur,d and dKv3.1 protein were absent in canine ventricular myocytes.

Structured PICO

Population

Dog atrial myocytes, canine ventricular myocytes, and Xenopus oocytes

Exposure

Cloning and heterologous expression of dKv3.1 (Shaw-type potassium channel)

Outcome

Molecular and electrophysiological characterization of dKv3.1 and its correlation with native IKur,dsurrogate

The Shaw-type potassium channel dKv3.1 is the likely molecular basis for the ultrarapid delayed rectifier current (IKur,d) in canine atrium.

Cite This Study

Yue et al. (2000) studied this question. dKv3.1 cloning and expression was evaluated on Molecular basis of IKur,d in dog atrium. The Shaw-type channel dKv3.1 is present in dog atrium, but not ventricle, and is the likely molecular basis of canine atrial ultrarapid delayed rectifier current (IKur,d).

synapsesocial.com/papers/6a6bd06426cff2e2f6f4832e https://doi.org/10.1111/j.1469-7793.2000.00467.x

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Molecular evidence for a role of Shaw (Kv3) potassium channel subunits in potassium currents of dog atrium

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Molecular evidence for a role of Shaw (Kv3) potassium channel subunits in potassium currents of dog atrium

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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