The relation of genetics to essential hypertension: a review.
Essential hypertension is fundamentally a genetic disease which emerges because of environmental impact. The genetic factors involve intracellular abnormalities which affect calcium metabolism within smooth muscle cells and possibly within the heart and sympathetic nervous system. These abnormalities are influenced by one or more proteins of which calmodulin is a candidate. Sodium pump abnormalities may be primary but may be secondary feedback effects. Homeostasis keeps the blood pressure and cardiac function normal, but eventually becomes less effective. Such homeostasis is produced by negative feedback, but positive external factors also influence the eventual results. Gross homeostasis is provided by the baroreceptors, the renin-angiotensin-aldosterone system, etc. The malfunction of any one or any combination of these systems may produce or accelerate hypertension. Hyperplasia and hypertrophy of arteriolar smooth muscle play their role but also multiply the genetic cellular defects. It is possible that in the early history of man essential hypertension had an advantage which now has become obsolete because normotensive man's potential lifespan has been increased by modern civilization.
D000818:Animals; D002118:Calcium / Q000378:metabolism; D002319:Cardiovascular System / Q000503:physiopathology; D004777:Environment; D006706:Homeostasis; D006801:Humans; D006973:Hypertension / Q000235:genetics*; D051381:Rats; D012964:Sodium / Q000097:blood; D013312:Stress, Physiological / Q000150:complications
D012964:Sodium; D002118:Calcium