Cushing's syndrome is a consequence of primary or, more commonly, secondary oversecretion of cortisol. Cardiovascular disease is the major cause of morbidity and mortality in Cushing's syndrome, and excess risk remains even in effectively treated patients. The cardiovascular consequences of cortisol excess are protean and include, inter alia, elevation of blood pressure, truncal obesity, hyperinsulinemia, hyperglycemia, insulin resistance, and dyslipidemia. This review analyses the relationship of cortisol excess, both locally and at tissue level, to these cardiovascular risk factors, and to putative mechanisms for hypertension. Previous studies have examined correlations between cortisol, blood pressure, and other parameters in the general population and in Cushing's syndrome. This review also details changes induced by short-term cortisol administration in normotensive healthy men.

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 erythropoie-tin concentration. (Hypertension. 2000;36:912-916.) Key Words: brain glucocorticoids hypertension, essential cortisol blood pressure H arvey W. Cushing (1869-1939) was a neurosurgeon who made important contributions to the physiology and pathophysiology of the pituitary gland. He was a pioneer in neurosurgical techniques and he played a leading role in reducing mortality from brain surgery. He is best remembered today for his description of the condition that bears his name, the glucocorticoid excess syndrome. The eponym is less commonly used for acoustic neuroma.

This study highlights differences between non-proteinuric pre-eclampsia and gestational hypertension. The subclassification of 'non-proteinuric pre-eclampsia' should be added to existing classification systems to alert clinicians to potential risks.