abstract

• The smooth muscle-walled blood vessels control blood pressure. The vessel lumen is lined by an endothelial cell (ECs) layer, interconnected to the surrounding smooth muscle cells (SMCs) by myoendothelial gap junctions. Gap junctions also maintain homo-cellular ECs-ECs and SMCs-SMCs connections. This gap junction network nearly equalises both cells%27 membrane potential and cytosolic ionic composition, whether in resting or stimulated conditions. When acetylcholine (ACh) activates ECs M3 receptors, a complex signalling cascade involving second messengers and ion channels is triggered to induce vasodilation.

authors

• Arreola Gómez Jorge

publication date

• 2024-01-01

funding provided via

• Consejo Nacional de Humanidades, Ciencias y Tecnologías, Conahcyt  Grant

published in

• Cell Calcium  Journal

keywords

• Arachidonic acid metabolites; K channels; Smooth muscle cells; TMEM16A; TRPV4; WNK kinase, Endothelial cells Acetylcholine; Animals; Arachidonic Acid; Endothelial Cells; Endothelium, Vascular; Gap Junctions; Humans; Ion Channels; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Receptor, Muscarinic M3; Signal Transduction; Vasodilation; acetylcholine; anoctamin 1; arachidonic acid; ion channel; potassium channel; protein kinase; protein kinase WNK; unclassified drug; vanilloid receptor 4; acetylcholine; arachidonic acid; ion channel; muscarinic M3 receptor; cell membrane potential; cytosol; endothelium; endothelium cell; gap junction; human; metabolite; nonhuman; Note; protein expression; pulmonary hypertension; smooth muscle cell; vasodilatation; animal; drug effect; endothelium cell; gap junction; metabolism; signal transduction; smooth muscle cell; vascular endothelium; vascular smooth muscle

Digital Object Identifier (DOI)

• 10.1016/j.ceca.2024.102904

PubMed ID

• 38728790

start page

end page

volume

• 121

issue