Remodeling of vascular smoth muscle ion channels involved in purinergic signaling in essential hypertension

Abstract

CaCCs Ca 2+-Activated Cl-Channels CaMKII Ca 2+ /Calmodulin-Dependent Protein Kinase II cAMP Cyclic Adenosine Monophosphate CFTR Cystic Fibrosis Transmembrane Conductance Regulator cGMP Cyclic Guanosine Monophosphate CGRP Calcitonin Gene-Related Peptide CHO Chinese Hamster Ovary Cell Line ClCa Cl-Channel Accessory Proteins ClCs Voltage-Gated Cl-Channels ClICs Intracellular Cl-Channels Cm Membrane Capacitance CO Cardiac Output CVP Central Venous Pressure DAG Diacylglycerol DIDS 4,4′-Diisothiocyanatostilbene-2,2′-Disulfonic Acid UDP Uridine Diphosphate UTP Uridine Triphosphate V clamp Voltage-Clamp Vm Membrane Potential VOCCs Voltage-Operated Ca 2+ Channels VPR Volume Pressure Recording VRACs Volume-Regulated Anion Channels VSM Vascular Smooth Muscle VSMCs Vascular Smooth Muscle Cells αβ-MeATP α,β-Methylene ATP Ca 2+ signaling Changes in [Ca 2+ ] i regulate many biological processes, such as muscle contraction, hormone secretion, gene expression and proliferation. Changes in [Ca 2+ ] i are regulated by the extracellular Ca 2+ influx, by Ca 2+ release from intracellular