Vasodilation is the process whereby blood vessels relax and widen, leading to an increase in blood flow and decrease in blood pressure. This mechanism is essential for maintaining tissue perfusion, regulating blood pressure, and ensuring efficient delivery of oxygen and nutrients. Vasodilation is regulated by molecular and signalling mechanisms involving interactions between endothelial cells and smooth muscle cells, along with the actions of neurotransmitters, hormones, and intracellular signalling pathways. The diffusible signalling gas nitric oxide (NO) is a critical vasodilator produced by endothelial cells through the action of endothelial nitric oxide synthase (eNOS). It diffuses into vascular smooth muscle cells, activating soluble guanylate cyclase (sGC), leading to an increase in levels of the second messenger cyclic guanosine monophosphate (cGMP). cGMP activates PKG, a serine/threonine kinase. PKG phosphorylates and activates potassium (K+) channels, which leads to K+ efflux from the smooth muscle cells, hyperpolarizing the membrane potential and decreasing contractility. In addition, PKG phosphorylates and inhibits myosin light chain kinase (MLCK), reducing its activity, resulting in decreased phosphorylation of myosin, and reduced contractile force, and additionally phosphorylates the regulatory subunit of myosin light chain phosphatase (MLCP), enhancing its activity in dephosphorylation of myosin, contributing to muscle relaxation. NO is stimulated by various factors, including shear stress, acetylcholine, and certain hormones. Prostacyclin is produced by endothelial cells and acts as a vasodilator. When prostacyclin binds to the IP receptor, it leads to the production of cyclic AMP (cAMP) and initiates downstream effects, such as vasodilation and inhibition of platelet aggregation. Endothelium-Derived Hyperpolarizing Factor (EDHF) is a term used to describe various endothelium-derived factors that cause hyperpolarization of vascular smooth muscle cells, leading to vasodilation. These factors include potassium ions, epoxyeicosatrienoic acids (EETs), and hydrogen peroxide. Adenosine is a molecule that is released in response to tissue hypoxia (low oxygen levels) and metabolic demand. It binds to adenosine receptors on vascular smooth muscle cells, leading to vasodilation. Activation of potassium channels in vascular smooth muscle cells leads to efflux of potassium ions, resulting in hyperpolarization and relaxation of the cells, which contributes to vasodilation. Bradykinin is a peptide released during tissue injury and inflammation. It binds to receptors on endothelial cells, leading to the release of NO and other vasodilators. Calcitonin Gene-Related Peptide (CGRP) is a neuropeptide released from sensory nerves that innervate blood vessels. It causes vasodilation by activating cAMP-dependent pathways in vascular smooth muscle cells. The parasympathetic nervous system is also involved in vasodilation and releases acetylcholine, which acts on muscarinic receptors in blood vessels, leading to vasodilation. The sympathetic nervous system, in contrast, releases norepinephrine that can cause either vasoconstriction or vasodilation, depending on the type of receptors activated and the tissue involved. During increased metabolic activity, tissues release metabolic by-products such as carbon dioxide and hydrogen ions. These factors can stimulate vasodilation to increase blood flow and oxygen delivery to metabolically active tissues. When blood pressure is elevated, baroreceptors in blood vessels signal to the brain to decrease sympathetic activity, leading to vasodilation and a decrease in blood pressure. We offer a wide product catalogue of research reagents for investigating vasodilation, including eNOS antibodies, NPY1R antibodies, Kininogen 1 antibodies, eNOS ELISA Kits, and Angiotensinogen ELISA Kits. Explore our full vasodilation product range below and discover more, for less. Alternatively, you can explore our Nitric Oxide Associated, Catecholamines, and Prostaglandins product ranges.