Glucocorticoids and blood pressure: a role for the cortisol/cortisone shuttle in the control of vascular tone in man.

@article{Walker1992GlucocorticoidsAB,
  title={Glucocorticoids and blood pressure: a role for the cortisol/cortisone shuttle in the control of vascular tone in man.},
  author={Brian R. Walker and A. A. Connacher and David John Webb and Christopher R. W. Edwards},
  journal={Clinical science},
  year={1992},
  volume={83 2},
  pages={
          171-8
        }
}
1. 11 beta-Hydroxysteroid dehydrogenase converts cortisol to inactive cortisone in man. In distal renal tubules, this inactivation protects mineralocorticoid receptors from cortisol. Congenital 11 beta-hydroxysteroid dehydrogenase deficiency and inhibition of 11 beta-hydroxysteroid dehydrogenase by liquorice or carbenoxolone result in cortisol-dependent hypokalaemia and hypertension. 2. 11 beta-Hydroxysteroid dehydrogenase is expressed in vascular smooth muscle. Both glucocorticoids and… 
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Alterations in cortisol metabolism in insulin-dependent diabetes mellitus: relationship with metabolic control and estimated blood volume and effect of angiotensin-converting enzyme inhibition.
TLDR
The present data suggest a chronic hyperglycemia-related impairment in the reduction of corticoids to tetrahydro metabolites and an imbalance in 11 beta HSD.
Hypertension and the cortisol-cortisone shuttle.
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Polymorphic variability in the HSD11B2 gene in part determines salt sensitivity, a forerunner for adult onset hypertension, and reduced placental 11 beta-HSD2 expression might underpin the Barker hypothesis, the epidemiological link between reduced birth weight and adult hypertension.
Increased vasoconstrictor sensitivity to glucocorticoids in essential hypertension.
TLDR
It is concluded that vasoconstrictor sensitivity to glucocorticoids is increased in essential hypertension and that this may initiate and/or sustain the increased peripheral vascular resistance that characterizes this disease.
Carbenoxolone increases hepatic insulin sensitivity in man: a novel role for 11-oxosteroid reductase in enhancing glucocorticoid receptor activation.
TLDR
It is inferred that carbenoxolone, by inhibiting hepatic 11 beta-reductase and reducing intrahepatic cortisol concentration, increases hepatic insulin sensitivity and decreases glucose production, and plasma cortisone provides an inactive pool that can be converted to active glucocorticoids at sites where 11 Beta-Reductase is expressed.
Clinical investigation of 11 beta-hydroxysteroid dehydrogenase.
TLDR
The underlying mechanism for all of these defects, and the putative role of endogenous inhibitors of 11 beta-OHSD, remains unclear, and measurement of the activity of individual isoforms should resolve this uncertainty.
11 alpha- and 11 beta-hydroxyprogesterone, potent inhibitors of 11 beta-hydroxysteroid dehydrogenase, possess hypertensinogenic activity in the rat.
TLDR
Results demonstrate that both 11 alpha- and 11 beta-hydroxyprogesterone are potently hypertensinogenic in the rat and that this activity depends on an intact adrenal and at least in part on the activation of mineralocorticoid receptors.
Endogenous 11 beta-hydroxysteroid dehydrogenase inhibitors and their role in glucocorticoid Na+ retention and hypertension.
TLDR
Results show that both 3 alpha,5B-THP and CDCA are hypertensinogenic in the rat and that the inhibition of either 11 beta-HSD2 or 11beta- HSD1 activity by endogenous progesterone metabolites and CD CA may be involved in the pathology of hypertension.
The role of 11 beta-hydroxysteroid dehydrogenase in the pathogenesis of hypertension.
Glycyrrhetinic acid attenuates vascular smooth muscle vasodilatory function in healthy humans.
TLDR
Disturbances in cortisol activity resulting from 11beta-HSD inactivation is a second plausible mechanism for mineralocorticoid-mediated hypertension in humans.
18 Cortisol Metabolism
TLDR
This chapter reviews current knowledge of enzymes which metabolize cortisol, and demonstrates altered peripheral metabolism of cortisol in obesity which may have important effects on tissue response to glucocorticoids.
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