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Article Review/Hyperlink
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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)
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