Endothelium, the new volume in the Advances in Pharmacology series, presents readers with a variety of chapters that cover various endothelium-derived mediators and their changes with gender, and during vascular development, senescence, and hypertensive disorders. Topics include endothelium, nitric oxide, gap junctions, potassium channels, endothelin, vascular development, vascular permeability, gender, aging, and preeclampsia. With contributions from the best authors in the field, the volume is an essential resource for pharmacologists, immunologists, and biochemists alike.

Vascular Pharmacology: Cytoskeleton and Extracellular Matrix, Volume 81, contains the latest information on the vascular cytoskeleton and extracellular matrix that is presented with helpful illustrations and supporting references by prominent scientists and highly-recognized experts in the vascular field. Topics of interest in this new release include Pharmacology of the Vascular Cytoskeleton and Extracellular Matrix, The Dynamic Actin Cytoskeleton in Smooth Muscle, The Role of the Actin Cytoskeleton in the Regulation of Vascular Inflammation, The Smoothelin Family of Proteins and the Smooth Muscle Cell Contractile Apparatus, Smooth Muscle Cytoskeletal Network Regulates Expression of the Profibrotic Genes PAI-1 and CTGF, and more.

Vascular Pharmacology: Smooth Muscle provides up-to-date information on the structure, function, signaling, and development of vascular smooth muscle. Contributors include prominent scientists and highly-recognized experts with major accomplishments in the field of vascular smooth muscle research.

Matrix Metalloproteinases and Tissue Remodeling in Health and Disease: Cardiovascular Remodeling, Volume 147 contains up-to-date information on the biology and function of matrix metalloproteinases and how their effects on tissue remodeling are altered in diseases of the cardiovascular, pulmonary, and musculoskeletal systems and in other tissues and organs, and in cancer. This latest release covers such highly evolving topics as Biochemical and Biological Attributes of Matrix Metalloproteinases, Matrix Metalloproteinases in Myocardial Infarction and Heart Failure, The Balance Between Metalloproteinases and TIMPs: Critical Regulator of Microvascular Endothelial Cell Function in Health and Disease, and Matrix Metalloproteinases and Platelet Function. As part of the Progress in Molecular Biology and Translational Science, users will find contributions from prominent scientists and highly-recognized experts who have major accomplishments in the research field of matrix metalloproteinases.

Matrix Metalloproteinases and Tissue Remodeling in Health and Disease: Target Tissues and Therapy, Volume, Volume 148, the latest volume in the Progress in Molecular Biology and Translational Science series covers a variety of timely topics, with chapters focusing on The Role of Matrix Metalloproteinases in Development, Repair, and Destruction of the Lungs, Matrix Metalloproteinases in Kidney Disease: Role in Pathogenesis and Potential as a Therapeutic Target, Regulation of Matrix Metalloproteinase in the Pathogenesis of Diabetic Retinopathy, Matrix Metalloproteinases in Normal Pregnancy and Preeclampsia, and Matrix Metalloproteinases, Neural Extracellular Matrix, and Central Nervous System Pathology. This volume is the second part of a thematic on matrix metalloproteinases and tissue remodeling in health and disease. It focuses on the role of MMPs in other systems, target tissues, and pathological disorders and the potential benefits of MMP inhibitors in various disorders.

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.