These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: [NO (nitric oxide) and its significance in regulation of vascular homeostasis]. Author: Kvasnicka T. Journal: Vnitr Lek; 2003 Apr; 49(4):291-6. PubMed ID: 12793052. Abstract: The endothelium is the largest autocrine and endocrine organ of the human organism. It participates in the regulation of the blood flow and tonus of the vascular wall, activation of thrombocytes, adhesion of monocytes to the vascular wall, thrombogenesis, lipid metabolism and growth of vessels. Endothelial cells may produce some 25 different biologically active substances. The most important one among them is probably NO. Under physiological conditions endothelial cells release permanently a small amount of NO or EDRF (endothelium-derived relaxing factor) and participate thus in the regulation of the tonus of the vascular wall at rest. The presence of NO excreated by endothelial cells can be detected in all parts of the circulation, from large arteries to small capillaries. Increased NO excretion is caused by a number of physiological stimuli, e.g. a rise of the blood pressure, drop of the partial oxygen pressure or the action of acetylcholine, ADP, ATP, thrombin, bradykinin or histamine. NO is a chemical messenger which is formed during oxidation of L-arginine to L-citrullin by the action of the enzyme NO synthase (NOS). Endothelial NOS is described as eNOS (endothelial/Type III/NOS-3). There exist also two other different isoforms of this enzyme: nNOS (neuronal/Type I/NOS-1/bNOS) andiNOS (inducible/Type II/NOS-2. NO plays an important part on the regulation of vascular homeostasis. It has a number of potential antiatherogenic functions. It causes vascular vasodilatation.[Abstract] [Full Text] [Related] [New Search]