[Membrane defect in primary arterial hypertension: a reflection of dysfunction of cellular oncogenes?].
A hypothesis is proposed, defining the basis of membrane defect associated with primary hypertension as alterations in the cell membrane oncogenes (protooncogenes), whose protein products are represented in the cell plasma membrane as receptors, cytoskeleton and ion transport regulating enzymes (protein kinases, phosphoinositide kinases), growth factors or similar substances. The proposition is based on a group of patterns, characteristic of primary hypertension and absent in its secondary forms, such as: Selective localization of initial alterations in cell plasmatic membranes; Enhanced proliferation of different cell types (vascular smooth muscles, myocardiocytes, blood cells, nerve cells, etc.) which is similar to the manifestation of the effect of tissue growth factors; Activated phosphoinositide metabolism in the cell plasmatic membrane; Imitation of the membrane defect, characteristic of primary hypertension, with the activation of protein kinase C.
Postnov
Iu V
IuV
D000818:Animals; D004910:Erythrocyte Membrane / Q000378:metabolism / Q000648:ultrastructure*; D005786:Gene Expression Regulation; D006801:Humans; D006973:Hypertension / Q000097:blood / Q000209:etiology* / Q000235:genetics; D009857:Oncogenes; D010716:Phosphatidylinositols / Q000378:metabolism; D011493:Protein Kinase C / Q000235:genetics / Q000378:metabolism; D051381:Rats; D011918:Rats, Inbred SHR
D010716:Phosphatidylinositols; D011493:Protein Kinase C
Membrannyĭ defekt pervichnoĭ srterial'noĭ gipertenzii: otrazhenie narushennoĭ funktsii kletochnykh onkogenov?