S-18-1: THE USUAL HEMODYNAMIC MECHANISM CAUSING SALT-INDUCED HYPERTENSION: ABNORMALLY INCREASED CARDIAC OUTPUT OR VASCULAR RESISTANCE?

Abstract

Two competing theories have been proposed for the hemodynamic mechanism that usually mediates salt sensitivity and the initiation of salt-induced hypertension. The historical natriuretic dysfunction theory holds that impaired renal excretion of sodium initiates hypertension by causing abnormally large increases in cardiac output secondary to abnormally large increases in salt and water retention. In contrast, the contemporary vasodysfunction theory holds that abnormal vascular resistance responses to salt, not abnormal increases in cardiac output, mediate salt sensitivity and the initiation of salt-induced hypertension. Primary aldosteronism is one of the most common causes of salt sensitivity and salt-dependent hypertension. This presentation will discuss new studies showing that hyperaldosteronism promotes salt sensitivity and initiation of salt-dependent hypertension by amplifying salt-induced increases in systemic vascular resistance, not cardiac output. The findings are consistent with the results of other studies showing that an abnormal vascular resistance response to salt (vasodysfunction) is also usually responsible for the initiation of salt-induced hypertension in humans and animals without hyperaldosteronism. The vasodysfunction framework for the pathogenesis of salt sensitivity and salt-induced hypertension has implications for: 1) understanding how various genetic and non-genetic factors influence BP responses to high salt diets, and 2) development of new methods for preventing and treating salt-dependent hypertension.