title: [Innovations in the postanalytical phase in clinical biochemistry. Functional heterogeneity of the arterial bed and pathogenesis of essential hypertension].
abstract: Early in phylogenesis during formation of paracrine-regulated communities of cells--the structural and functional units of future organs--each of them comprised a pool of specialized cells, interstitial tissue elements, and a local peristaltic pump. The pump within the community fulfilled the biological functions of homeostasis and the endoenvironment (intercellular environment purity). This community is, say, the nephron that consists of a renal capillary, interstitial tissue, and an afferent arteriole. The renal capillary cells regulate the activity of a muscle arteriole (a local pump) on the basis of glomerulotubular direct coupling and feedback to give rise to municipal regulation. Later on, the heart and elastic arteries pooled million local peristaltic pumps that operated over ages. Phylogenetically, the arterial bed comprises two portions: proximal (the heart + elastic arteries) and distal (muscle arterioles). Regulation of the proximal arterial bed takes place at the federal level; this is accomplished by the vasomotor center via sympathetic and parasympathetic innervation. Control of the distal arterial bed, the peripheral peristaltic pumps, is exercised by municipal regulation at the level of paracrine communities. When the biological functions of homeostasis and the endoenvironment are realized, federal regulation comes into conflict with municipal one; this imbalance is implicated in the pathogenesis of essential hypertension. Blood pressure measurement provides data on the state of the proximal arterial bed and the endothelium-dependent vasodilation test characterizes the state of the distal portion and that of peripheral peristaltic pumps and muscle arterioles. Confrontation of federal and municipal regulations in the nephron paracrine community is a principal cause of arterial hypertension, glomerulosclerosis, or tubulointerstitial inflammation.
authors.forename: V N
authors.initials: VN
authors.lastname: Titov
mesh_terms: D000818:Animals; D001158:Arteries / Q000503:physiopathology*; D005075:Biological Evolution; D001775:Blood Circulation; D004730:Endothelium, Vascular / Q000503:physiopathology; D006801:Humans; D006973:Hypertension / Q000209:etiology / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D019899:Paracrine Communication; D010802:Phylogeny; D014664:Vasodilation