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Cortisol inhibits cholinergic vasodilation in the human forearm
G J Mangos1, B R Walker, J J Kelly
1Department of Medicine, St George Hospital, University of New South Wales, Kogarah, Australia. g.mangos@unsw.edu.au
American Journal of Hypertension
|November 15, 2000
Summary
Exogenous cortisol impairs blood vessel dilation in response to acetylcholine, suggesting nitric oxide system abnormalities contribute to hypertension in glucocorticoid-treated individuals.
Area of Science:
- Cardiovascular Physiology
- Endocrinology
- Hypertension Research
Background:
- Exogenous cortisol increases blood pressure (BP) in humans.
- Glucocorticoid activity abnormalities are linked to essential hypertension.
- The effect of cortisol on vascular responses requires further investigation.
Purpose of the Study:
- To test if exogenous cortisol attenuates the cholinergic dilator response in forearm circulation.
- To investigate the role of the nitric oxide system in cortisol-induced vascular dysfunction.
Main Methods:
- Randomized, double-blind, crossover study in 14 healthy men.
- Forearm venous plethysmography used to measure forearm blood flow.
- Responses to acetylcholine and sodium nitroprusside assessed pre- and post-NG-monomethyl-L-arginine after cortisol or placebo administration.
Main Results:
- Exogenous cortisol increased systolic BP and suppressed serum cortisol.
- Cholinergic vasodilation was impaired after 5 days of cortisol administration (P < .05).
- Cortisol did not affect responses to sodium nitroprusside; NG-monomethyl-L-arginine's effect was blocked by cortisol.
Conclusions:
- Exogenous cortisol impairs cholinergic vasodilation in human forearm circulation.
- The endothelial nitric oxide system is implicated in the mechanism of impaired cholinergic dilation under glucocorticoid treatment.
- Findings suggest a potential link between glucocorticoid excess and endothelial dysfunction in hypertension.