Role of Kv7 Channels in Vascular Dysfunction associated with Metabolic Syndrome
- Author:
Sewon LEE
1
Author Information
- Publication Type:Review
- Keywords: K+ channels; Retigabine; Linopirdine; Flupirtine; Vasorelaxation
- MeSH: Animals; Aorta; Blood Vessels; Calcium; Cell Membrane; Diabetes Mellitus; Humans; Hypertension; Ion Channels; Membrane Potentials; Mice; Models, Animal; Muscle, Smooth, Vascular; Potassium; Rats; Rats, Inbred SHR; Renal Artery; Vasoconstriction; Vasodilation
- From:Korean Journal of Obesity 2016;25(1):10-15
- CountryRepublic of Korea
- Language:Korean
- Abstract: Vasoconstriction is regulated by various ion channels expressed in the plasma membrane of vascular smooth muscle cells. In particular, potassium (K+) channel activity determines resting membrane potential and regulates intracellular calcium (Ca2+) signaling. A number of studies have suggested that dysregulation of K+ channel activity is associated with increased myogenic tone or diminished vasorelaxation. Among the various families of K+ channels, voltage-dependent K+ channels (Kv channels) encoded by the KCNQ gene family (Kv7 channels or M channels) are widely expressed in various blood vessels isolated from mouse, rat, and human. Recent studies have demonstrated that a subunit of the Kv7 channel, Kv7.4, is down-regulated in the aorta and mesenteric and renal arteries of the Spontaneously Hypertensive Rat (SHR) model. Previous studies have also suggested that Kv7 channels play an important role in the regulation of vasorelaxation/vasoconstriction in response to activators/blockers. In addition, previous studies have indicated that hypertension, diabetes mellitus, and cerebrovascular disease result in development of vascular dysfunction associated with Kv7 abnormalities in various animal models. This review focuses on the potential role of the Kv7 channel in vascular dysfunction.
