Hypertension, Vol 23, 381-394, Copyright © 1994 by American Heart Association
JE Hall
In all forms of hypertension, including human essential hypertension,
pressure natriuresis is reset to higher blood pressures. Because human
essential hypertension is a heterogeneous disease, it is likely that there
are multiple neurohumoral and intrarenal causes of abnormal pressure
natriuresis and increased blood pressure. Weight gain is recognized to be
an important contributor to essential hypertension, although the mechanisms
that link obesity with altered renal function and high blood pressure have
not been fully elucidated. In obese dogs and humans, the shift of pressure
natriuresis to higher blood pressures appears to be due mainly to increased
tubular reabsorption, as glomerular filtration rate and renal plasma flow
are increased compared with normal. Multiple causes of increased tubular
reabsorption and hypertension in obesity have been postulated, including
insulin resistance and hyperinsulinemia, activation of the sympathetic
nervous and renin-angiotensin systems, and physical changes within the
kidney itself. Support for the insulin resistance-hyperinsulinemia link
between obesity and hypertension has been inferred mainly from acute and
epidemiologic studies showing a correlation between insulin and blood
pressure. Recent studies suggest that chronic hyperinsulinemia, comparable
to that found in obesity, cannot account for obesity hypertension in dogs
or humans. Activation of the sympathetic nervous system may play a role in
obesity-induced hypertension, and there is evidence for a role of altered
intrarenal physical forces caused by histological changes within the renal
medulla. The quantitative importance of each of these abnormalities in
altering renal function and raising blood pressure in obesity remains to be
determined but is an important area of research for understanding human
essential hypertension.
ARTICLES
Louis K. Dahl Memorial Lecture. Renal and cardiovascular mechanisms of hypertension in obesity
Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson 39216-4505.
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