Inverting Notions of the Biological Role of the Renin → Angiotensin-II → Aldosterone System and the Function of Arterial Pressure as a Metabolism Regulator
Authors: Vladimir N. Titov
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The phylogenetic theory of general pathology postulates that notions of the biological role of arterial pressure (AP) in physiology and pathology have been subjected to inversion. The nephron’s activation of the synthesis of the components renin → angiotensin-II (A-II) and the augmentation of aldosterone secretion are directed not at an increase in AP but at preserving the volume of the piece of the third world ocean, privatized by each species, - the pool of the intercellular milieu in which, just like millions of years before, there continue to live all cells. Phylogenetically earlier organs cannot regulate the action of a later one in AP phylogenesis – a physical factor in metabolism regulation. It is not the kidneys that increase AP but the vasomotor center, which, increasing AP in the proximal segment and further hydrodynamic pressure in the distal segment of the arterial bed, seeks to reanimate the function of nephrons, the biological function of endoecology and the biological reaction of excretion. In addition to playing a major role in the biological function of locomotion, AP is a physical factor in compensating for impairments in the biological functions of homeostasis, trophology, endoecology, and adaptation. There have formed sequentially three levels of metabolic regulation in phylogenesis. At an autocrine level, there occurs a specific regulation of biochemical reactions. Within paracrinally regulated communities of cells, in the distal segment of the arterial bed, metabolism is regulated by millions of local peristaltic pumps through compensating for the biological reaction of endothelium-dependent vasodilation, microcirculation, and the action of humoral mediators and hormonal principles. In vivo from the level of the vasomotor center metabolism is non-specifically, systemically regulated by the physical factor – AP – through sympathetic activation of the heart; in the proximal segment of the arterial bed and the distal one, AP, overcoming the resistance, virtually “collapses” arterioles with impaired microcirculation. A-II acts as a vasoconstrictor only in the distal segment of the arterial bed. In the pathogenesis of essential, metabolic AH, the paracrine communities of the nephron and the kidney are involved in the realization of pathological compensation secondarily and are often “wrongfully accused”, just like the other “target organs” – the brain, the lungs, and the heart.