August 22, 2015AJP Heart and Circulatory Physiology

Small-conductance Ca²⁺-activated K⁺ current is upregulated via the phosphorylation of CaMKII in cardiac hypertrophy from spontaneously hypertensive rats

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Population

Normotensive Wistar-Kyoto rats and spontaneous hypertensive rats

Comparison

Apamin and KN-93 vs Normotensive WKY rats vs SHRs; baseline vs drug…

Design

Preclinical

Authors

KMKazuya MizukamiHokkaido hospital HYHisashi YokoshikiElectrophysiology HMHirofumi MitsuyamaNakamura Memorial Hospital

Discussion

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Implication

May identify SK-CaMKII axis as antiarrhythmic target in LVH; leaves open clinical translation from animal data.

Structured PICO

Population

Normotensive Wistar-Kyoto (WKY) rats and spontaneous hypertensive rats (SHRs) (n=6 per group for patch-clamp and Western blot)

Intervention

Apamin (100 nM, SK channel blocker) and KN-93 (1 μM, CaMKII inhibitor)

Comparator

Normotensive WKY rats vs SHRs; baseline vs drug exposure

Outcome

Apamin-sensitive K(+) current (IKAS) and SK channel protein isoform expression (SK1, SK2, SK3)surrogate

SK channels are upregulated via enhanced CaMKII activation in hypertensive cardiac hypertrophy, providing a potential molecular mechanism for ventricular arrhythmias in this setting.

Cite This Study

Mizukami et al. (2015) studied this question.

synapsesocial.com/papers/6a737e53d3d4e530dbfb6787 https://doi.org/10.1152/ajpheart.00825.2014

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Small-conductance Ca²⁺-activated K⁺ current is upregulated via the phosphorylation of CaMKII in cardiac hypertrophy from spontaneously hypertensive rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Small-conductance Ca²⁺-activated K⁺ current is upregulated via the phosphorylation of CaMKII in cardiac hypertrophy from spontaneously hypertensive rats

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider