[The molecular and physiological aspects of endothelial dysfunction. The role of endogenous chemical regulators].
Monolayer of endothelial cells that cover the vascular channels are the major regulator of haemo-vascular homeostasis. Endothelium secretes the chemical factors that affect contraction of the muscular vascular cells, permeability of tissue, blood fluidity, intercellular interaction in vascular structure of the channel as a whole and of different regions. In its turn, the secretory function of endothelial cells is stimulated by mechanical or hormonal factors under a feedback system principle. Special features of morphology and biochemistry of vascular endothelium cells determine the micro-organs heterogeneity of the vascular channel depending on phenotine, gene expression, size and growth of endothelium cells. On this basis the processing biochemical disintegration develop either selectively or in a generalised form, and results in development of endothelial dysfunctions, as the original factor of many cardiovascular pathologies. Endothelial disfunction is a systemic pathology related to pathology of microstructure and hormonal function of endothelial cells representing a major tissue system of the vascular channel. Formation of hypertension states, ischemic cardiopathology, haemostasis changes, metabolic pathology (hypercholesterinemia and hyperglycemia) that lead to pathogenesis of arteriosclerosis, diabetes (etc.) as result of modified function of endothelium, and above all, pathology of production by dilator and constrictor substances, and the factors regulating interaction of endothelium with blood cells. The basic mechanism for development of the endothelial dysfunction is related to modification of synthesis and releasing of nitrogen oxide, a key regulator of the endothelial-vasal system. Physiologically active peptides (angiotensin II, endothelin-I, bradykinin, adrenomedullin and ANP) contribute to development of the processes related to the endothelium function and dysfunction. An important role is played, apparently, by growth peptide factors and specific proteins of cellular adhesion and membrane interaction--to integrins and selectins.
Gomazkov
O A
OA
Research Institute of Biomedical Chemistry, Russian Academy of Medical Sciences, Moscow.
D000818:Animals; D001161:Arteriosclerosis / Q000209:etiology / Q000503:physiopathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000503:physiopathology*; D006331:Heart Diseases / Q000209:etiology / Q000503:physiopathology; D006706:Homeostasis / Q000502:physiology; D006801:Humans; D018377:Neurotransmitter Agents / Q000502:physiology*; D009569:Nitric Oxide / Q000502:physiology; D014652:Vascular Diseases / Q000175:diagnosis / Q000209:etiology / Q000503:physiopathology
D018377:Neurotransmitter Agents; D009569:Nitric Oxide