HDCN Article Review/Hyperlink

Walker BR, Best R, Shackleton CHL, Padfield PL, Edwards CRW

Increased vasoconstrictor sensitivity to glucocorticoids in essential hypertension

Hypertension (Feb) 27:190-196 1996

Hypercortisolism is known to cause hypertension in patients with Cushing s syndrome. Recent data indicate that glucocorticoids, such as cortisol, could increase blood pressure by binding to mineralocorticoid receptors as a result of altered receptor affinity or because of genetic deficiency or functional inactivation activation of 11 -hydroxysteroid dehydrogenase. However, it is also possible that increased vasomotor tone in hypertension could be mediated in part by an increase in sensitivity to glucocorticoids. Topical glucocorticoids can induce vasoconstriction when applied topically to the skin which is the basis for a technique to assay glucocorticoid responsiveness in asthmatics.

In this paper the authors used this dermal assay to determine whether patients with essential hypertension have increased vasoconstrictor sensitivity to glucocorticoids. They compared the dermal vasoconstrictor response to increasing concentrations of both beclomethasone proprionate and cortisol in 11 normotensive controls and 11 hypertensives (4 of whom were on antihypertensive medications). In addition, they measured plasma half-life of 3H- cortisol, dexamethasone suppression and urinary free cortisol. They found that the dermal vasoconstrictor response was increased in hypertensives; however, there was no difference in dexamethasone suppression of endogenous cortisol. Plasma half-life of 3H- cortisol was increased and urinary free cortisol was decreased in hypertensives as compared with controls.

The authors conclude that the increased vasoconstrictor response in hypertensives is due to an increase in sensitivity to cortisol. Also, they suggest that this response may play a role in the pathogenesis of hypertension in both Cushing s syndrome and essential hypertension. The findings are provocative and interesting particularly in light of recent advances in our understanding of steroid hormone metabolism in cardiovascular diseases, especially hypertension. However, the relevance of this finding is still in question and whether it is of significance in the pathogenesis of hypertension remains unclear. The dermal vessel vasoconstrictor sensitivity to these corticosteroids does not necessarily translate into a generalized effect that could be responsible for increasing blood pressure in Cushing s syndrome or essential hypertension. Although more difficult to study, it would be important to demonstrate increased sensitivity to vasoconstriction in other vascular beds including the kidney. (Robert D. Toto, M.D., University of Texas Southwestern Medical Center)