TY - BOOK ID - 8285182 TI - Regulation of vascular smooth muscle function PY - 2010 SN - 161504180X 1615041818 PB - [San Rafael, Calif.?] : Morgan & Claypool Life Sciences, DB - UniCat KW - Muscle contraction. KW - Vascular diseases. KW - Vascular smooth muscle. KW - Ion Channels KW - Muscle Proteins KW - Microfilament Proteins KW - Hemodynamics KW - Muscle, Smooth KW - Molecular Motor Proteins KW - Cardiovascular Diseases KW - Blood Vessels KW - Diseases KW - Muscles KW - Contractile Proteins KW - Cardiovascular Physiological Processes KW - Cardiovascular System KW - Adenosine Triphosphatases KW - Membrane Glycoproteins KW - Biopolymers KW - Membrane Transport Proteins KW - Cytoskeletal Proteins KW - Polymers KW - Tissues KW - Carrier Proteins KW - Acid Anhydride Hydrolases KW - Proteins KW - Cardiovascular Physiological Phenomena KW - Membrane Proteins KW - Anatomy KW - Musculoskeletal System KW - Amino Acids, Peptides, and Proteins KW - Circulatory and Respiratory Physiological Phenomena KW - Macromolecular Substances KW - Hydrolases KW - Chemicals and Drugs KW - Phenomena and Processes KW - Enzymes KW - Enzymes and Coenzymes KW - Myosins KW - Muscle, Smooth, Vascular KW - Vasoconstriction KW - Calcium Channels KW - Vascular Diseases KW - Human Anatomy & Physiology KW - Health & Biological Sciences KW - Physiology KW - Vascular resistance. KW - Blood pressure. KW - Vascular smooth muscle KW - Physiology. KW - physiology. KW - Signal transduction KW - Calcium KW - Blood pressure KW - AngII, angiotensin II KW - ATP, adenosine triphosphate KW - CPI-17, PKC-potentiated phosphatase inhibitor protein-17 kDa KW - CAM, calmodulin KW - DAG, diacylglycerol KW - ET-1, endothelin KW - IP3, inositol 1,4,5-trisphosphate KW - MAPK, mitogen-activated protein kinase KW - MARCKs, myristoylated alanine-rich C-kinase substrate KW - MEK, MAPK kinase KW - MLC, myosin light chain KW - NCX, Na+-Ca2+ exchanger KW - PDBu, phorbol 12,13-dibutyrate; PIP2, phosphatidylinositol 4,5-bisphosphate KW - PKC, protein kinase C KW - PMA, phorbol myristate acetate KW - RACKs, receptors for activated C-kinase KW - ROCK, Rho-kinase KW - VSMC, vascular smooth muscle cell UR - https://www.unicat.be/uniCat?func=search&query=sysid:8285182 AB - Vascular smooth muscle (VSM) constitutes most of the tunica media in blood vessels and plays an important role in the control of vascular tone. Ca2+ is a major regulator of VSM contraction and is strictly regulated by an intricate system of Ca2+ mobilization and Ca2+ homeostatic mechanisms. The interaction of a physiological agonist with its plasma membrane receptor stimulates the hydrolysis of membrane phospholipids and increases the generation of inositol 1,4,5-trisphosphate (IP3) and diacylglycerol (DAG). IP3 stimulates Ca2+ release from the intracellular stores in the sarcoplasmic reticulum. Agonists also stimulate Ca2+ influx from the extracellular space via voltage-gated, receptor-operated, and store-operated channels. Ca2+ homeostatic mechanisms tend to decrease the intracellular free Ca2+ concentration ([Ca2+]i) by activating Ca2+ extrusion via the plasmalemmal Ca2+ pump and the Na+/Ca2+ exchanger and the uptake of excess Ca2+ by the sarcoplasmic reticulum and possibly the mitochondria. A threshold increase in [Ca2+]i activates Ca2+-dependent myosin light chain (MLC) phosphorylation, stimulates actin-myosin interaction, and initiates VSM contraction. The agonist-induced maintained increase in DAG also activates specific protein kinase C (PKC) isoforms, which in turn cause phosphorylation of cytoplasmic substrates that increase the contractile myofilaments force sensitivity to Ca2+ and thereby enhance VSM contraction. Agonists could also activate Rho kinase (ROCK), leading to inhibition of MLC phosphatase and further enhancement of the myofilaments force sensitivity to Ca2+. The combined increases in [Ca2+]i, PKC and ROCK activity cause significant vasoconstriction and could also stimulate VSM hypertrophy and hyperplasia. The protracted and progressive activation of these processes could lead to pathological vascular remodeling and vascular disease. ER -