Vasoregulation at the molecular level: a role for the beta1 subunit of the calcium-activated potassium (BK) channel.
Essential hypertension is among the most common and most costly medical conditions in the United States. Multiple defects in the kidneys, the vasculature, and the neuro-endocrine system may contribute to the development of this disorder. Within the past decade investigators have identified several molecular components of the vasculature that control tone and influence blood pressure. For example, the large conductance BK type calcium-activated potassium channel has recently been shown to play an important role in maintaining the dynamic equilibrium between vasoconstriction and vasodilation of vascular smooth muscle. Activation of vascular smooth muscle BK channels leads to hyperpolarization of the cell membrane, which causes deactivation of voltage-dependent calcium channels and vasodilation. In this review, we will summarize recently published data focusing on the role of the BK channel's accessory beta1 subunit as well as other modulators of BK channel activation that influence vascular tone and blood pressure.
Patterson
Andrew J
AJ
Department of Anesthesia, Stanford University Medical Center, CA 94305-5640, USA. ajpanes@leland.stanford.edu
Henrie-Olson
Jenifer
J
Brenner
Robert
R
D000818:Animals; D001794:Blood Pressure / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism; D006801:Humans; D006973:Hypertension / Q000503:physiopathology*; D051379:Mice; D009131:Muscle, Smooth, Vascular; D024681:Potassium Channels, Calcium-Activated / Q000502:physiology*; D019837:Ryanodine Receptor Calcium Release Channel / Q000378:metabolism; D014661:Vasoconstriction / Q000502:physiology; D014664:Vasodilation / Q000502:physiology
D024681:Potassium Channels, Calcium-Activated; D019837:Ryanodine Receptor Calcium Release Channel; D002118:Calcium