(Hypertension. 2000;36:912.)
© 2000 American Heart Association, Inc.
Colin Johnston - A Celebration |
Cushing, Cortisol, and Cardiovascular Disease
From John Curtin School of Medical Research, The Australian National University, Canberra, ACT (J.A.W.); and the Departments of Medicine and Renal Medicine, St George Hospital, University of New South Wales, Kogarah, NSW (G.J.M., J.J.K.).
Correspondence to Judith A. Whitworth, John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2601.
Abstract—Cushing’s syndrome of glucocorticoid excess is named after the eminent Boston neurosurgeon Harvey W. Cushing (1869-1939). The recognition that glucocorticoid excess produces hypertension led to examination of the role of cortisol in essential hypertension, but it is only over the last decade that evidence has emerged to support the concept. Despite the widespread assumption that cortisol raises blood pressure as a consequence of renal sodium retention, there are few data consistent with the notion. Although it has a plethora of actions on brain, heart and blood vessels, kidney, and body fluid compartments, precisely how cortisol elevates blood pressure is unclear. Candidate mechanisms currently being examined include inhibition of the vasodilator nitric oxide system and increases in vasoconstrictor erythropoietin concentration.
Key Words: brain • glucocorticoids • hypertension, essential • cortisol • blood pressure
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