Developing the idea of the membrane origin of primary hypertension, we proceed from the following: this form of hypertension is based on widespread (i.e., not limited to one type of cells) abnormalities in the ion transport function of the plasma membrane and its structure, leading to changes in the, values of several constants regulated by the plasma membrane (in particular, pH(i), Ca(i)2+); plasma membrane alterations apparently have a genomic source and are initiated by a factor whose impact is mediated by the protooncogenes of the genome: the specific functions of the cell are preserved in these conditions by means of a mechanism of cell adaptation, revealed in the example of adipose tissue and called <<cell resetting>>; the development of cell resetting simultaneously initiates changes in hormone-target relations which manifest themselves, in particular, in augmented corticosteroid secretion (adrenal cortex hypertrophy), in increased activity of the sympathetic nervous system, and in the phenomenon of hyperinsulinemia; considering membrane alterations as the source of primary hypertension, the author proceeds from the assumption of the role of the blood ciruclation system as an <<intermediate link>> between two basic systems (effectors) of water-salt homeostasis at the cellular level and at the level of the whole body, i.e., between the cell plasma membrane and the kidney; under conditions of <<membrane defect>> the functional equilibrium indicated in the previous item occurs at a new level of hormone-target interaction and is achieved via the development of chronic arterial hypertension and the kidney resetting (kidney shifting after Guyton) that prevents water and salt loss. Thus, increased blood pressure (hypertension) in the author s understanding is an inherent feature of the equilibrium occurring under conditions of ''membrane defect'', between two water-salt homeostasis systems of different levels, i.e., the plasma membrane and the kidney.
