March 19, 2009British Journal of PharmacologyOpen Access

Endothelial Ca²⁺‐activated K⁺channels in normal and impaired EDHF–dilator responses – relevance to cardiovascular pathologies and drug discovery

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Structured PICO

Population

Endothelial KCa3.1 and KCa2.3 channels in normal physiology, KCa3.1/KCa2.3-deficient mice, and cardiovascular disease states (hypertension, diabetes, dyslipidemia, atherosclerosis)

Intervention

KCa3.1/KCa2.3 openers

Endothelial KCa3.1 and KCa2.3 channels are critical for EDHF-mediated vasodilation and blood pressure control, representing potential novel targets for antihypertensive drug discovery.

Authors

IGIvica GrgicPhilipps University of Marburg BKBrajesh P. KaisthaAstraZeneca (United Kingdom)JHJoachim HoyerPhilipps University of Marburg

Discussion

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Implication

May support KCa channel targeting for hypertension; leaves open human translation and trial design.

Cite This Study

Grgic et al. (2009) studied this question.

synapsesocial.com/papers/6a092ce01d1abd907d1608d5 https://doi.org/10.1111/j.1476-5381.2009.00132.x

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Endothelial Ca²⁺‐activated K⁺channels in normal and impaired EDHF–dilator responses – relevance to cardiovascular pathologies and drug discovery

Structured PICO

Discussion

Implication

Cite This Study

Endothelial Ca²⁺‐activated K⁺channels in normal and impaired EDHF–dilator responses – relevance to cardiovascular pathologies and drug discovery

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider