PATHOGENESIS OF ESSENTIAL HYPERTENSION

  • 1 January 1978
    • journal article
    • review article
    • Vol. 1  (2) , 171-197
Abstract
Essential hypertension is a quantitative abnormality; the pathological effects and risks increase with the blood pressure level. In Western countries blood pressure rises with age in most individuals; essential hypertension is more frequent in middle and older age groups. An individual''s blood pressure level is probably determined by many interacting factors including heredity, which probably acts multifactorially, and many environment influences, including psychological stress and obesity. Specific factors may be of varying importance in different individuals and in different populations. Several physiological mechanisms control the blood pressure level and may be altered in essential hypertension. In early hypertension sympathetic nervous activity is sometimes increased. In long-standing hypertension this is less marked. Cardiac output may be increased in borderline hypertension but is normal in established hypertension when total peripheral resistance is increased. Total exchangeable Na is normal; the renal pressure-natriuresis balance is altered so that for a given pressure the hypertensive kidney excretes less Na. In some patients plasma renin is low, probably due to renal adaption to prolonged hypertension. The pathogenic sequence in essential hypertension is uncertain. Increased autonomic activity may cause vasoconstriction in renal and other arterioles and increase cardiac output leading to a rise in blood pressure. Elevated pressure itself produces structural changes in the resistance vessels including those of the kidney, which eventually maintain the hypertension even when the initiating stimulus is removed. The way in which heredity and environment influence pathogenic mechanism is uncertain. Heredity might influence the autonomic response to stress or the liability to irreversible changes in the resistance vessels or in the kidney. Environmental factors may increase autonomic activity, enhance vascular reactivity or alter renal function.