Aetiology of hypertension.
We are still uncertain of the way in which environment and heredity interact to produce increased arterial pressure in patients with essential hypertension. Few indisputable abnormalities can be demonstrated. Of these there is universal agreement that structural vessel hypertrophy is present and this acts probably as a maintenance and perhaps amplifying system resulting from an initial increase in arterial pressure. It cannot of course explain an increase in arterial pressure ab initio. Most of the well defined systems of arterial pressure control do not show any marked abnormality, although there is some evidence for a modest degree of sympathetic nervous system overactivity. Although some of the changes in cation fluxes across erythrocyte and leucocyte membranes are still debatable, there is general agreement that cation handling by erythrocytes and leucocytes is abnormal in many patients with essential hypertension and that some of these abnormalities are shared by the normotensive relatives of hypertensive patients. The most promising approach is that there is an abnormality of the cell membrane vascular smooth muscle which is partly genetically determined and perhaps also involves the autonomic nervous system. This produces an increased pressor response to environmental stimuli which becomes perpetuated and perhaps amplified by structural hypertrophy of the resistance vessels.
D000818:Animals; D001341:Autonomic Nervous System / Q000503:physiopathology; D001692:Biological Transport; D001794:Blood Pressure; D002462:Cell Membrane / Q000502:physiology; D004285:Dogs; D006801:Humans; D006973:Hypertension / Q000209:etiology* / Q000503:physiopathology; D009131:Muscle, Smooth, Vascular / Q000503:physiopathology; D051381:Rats; D012084:Renin-Angiotensin System; D012964:Sodium / Q000378:metabolism; D014882:Water-Electrolyte Balance
D012964:Sodium