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Br J Pharmacol. 2015 Sep;172(18):4493-4505. doi: 10.1111/bph.13234. Epub 2015 Jul 24.

Genetic deficit of K.

British journal of pharmacology

Christine Wandall-Frostholm, Thomas Dalsgaard, Vytis Bajoriūnas, Aida Oliván-Viguera, Veeruanjaneyulu Sadda, Lilliana Beck, Susie Mogensen, Edgaras Stankevicius, Ulf Simonsen, Ralf Köhler

Affiliations

  1. Department of Biomedicine, Pulmonary and Cardiovascular Pharmacology, Aarhus University, Aarhus, Denmark.
  2. Department of Physiology and Pharmacology, Faculty of Medicine, Kaunas, Lithuania.
  3. Aragon Institute of Health Sciences IIS and ARAID, Zaragoza, Spain.

PMID: 26102209 PMCID: PMC4562510 DOI: 10.1111/bph.13234

Abstract

BACKGROUND AND PURPOSE: The intermediate conductance calcium/calmodulin-regulated K

EXPERIMENTAL APPROACH: An opener of TRPV4 channels, GSK1016790A, was infused in wild-type (wt) and K

KEY RESULTS: In wt mice, GSK1016790A decreased right ventricular and systemic pressure leading to a fatal circulatory collapse that was accompanied by increased protein permeability, lung haemorrhage and fluid extravasation. In contrast, K

CONCLUSIONS AND IMPLICATIONS: Our findings show that a genetic deficiency of K

© 2015 The British Pharmacological Society.

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