The Management of Primary Aldosteronism: Case Detection, Diagnosis, and Treatment: An Endocrine Society Clinical Practice Guideline.
This guideline recommends that all patients with primary aldosteronism undergo adrenal computed tomography as the initial study in subtype testing and to exclude adrenocortical carcinoma and advises that an experienced radiologist should establish/exclude unilateral primary aldehydes using bilateral adrenal venous sampling.
Case detection, diagnosis, and treatment of patients with primary aldosteronism: an endocrine society clinical practice guideline.
- J. Funder, R. Carey, V. Montori
- MedicineJournal of Clinical Endocrinology and Metabolism
- 1 September 2008
The Task Force developed clinical practice guidelines for the diagnosis and treatment of patients with primary aldosteronism and recommended that patients with bilateral adrenal hyperplasia, or those unsuitable for surgery, optimally be treated medically by mineralocorticoid receptor antagonists.
Mineralocorticoid action: target tissue specificity is enzyme, not receptor, mediated.
The presence of the enzyme 11 beta-hydroxy-steroid dehydrogenase, which converts cortisol and corticosterone, but not aldosterone, to their 11-keto analogs, means that these analogs cannot bind to mineralocorticoid receptors.
Outcomes after adrenalectomy for unilateral primary aldosteronism: an international consensus on outcome measures and analysis of remission rates in an international cohort.
- T. Williams, J. Lenders, M. Reincke
- MedicineThe Lancet Diabetes and Endocrinology
- 1 September 2017
Proopiomelanocortin processing in the pituitary, central nervous system, and peripheral tissues.
To yield biologically active products, precursors commonly undergo a series of highly organized posttranslational events, including selective proteolytic cleavage and other enzymatic modifications which take place within specific membrane-bounded compartments.
Glucocorticoid and mineralocorticoid receptors: biology and clinical relevance.
- J. Funder
- Biology, MedicineAnnual Review of Medicine
- 1997
Physiological roles for aldosterone and glucocorticoid membrane receptors, and for the recently described nuclear receptors for 11-ketosteroids in 11 beta-hydroxysteroid dehydro-genase-protected epithelia, remain to be established.
Dehydroepiandrosterone increases endothelial cell proliferation in vitro and improves endothelial function in vivo by mechanisms independent of androgen and estrogen receptors.
- Maro R I Williams, T. Dawood, P. Komesaroff
- Biology, MedicineJournal of Clinical Endocrinology and Metabolism
- 1 September 2004
DHEA increases EC proliferation in vitro by mechanism(s) independently of either androgen receptor or estrogen receptor and in vivo enhances large and small vessel EC function in postmenopausal women.
Mineralocorticoid Receptors: Distribution and Activation
- J. Funder
- Biology, MedicineHeart Failure Reviews
- 2005
Cortisol changes from an MR antagonist to an MR agonist when intracellular redox state is changed—by inhibition of 11β HSD2, generation of reactive oxygen species, or intrace cellular introduction of oxidised glutathione (GSSG)—cortisol appears to underlie the therapeutic efficacy of MR blockade in heart failure and in essential hypertension.
Deletion of Mineralocorticoid Receptors From Macrophages Protects Against Deoxycorticosterone/Salt-Induced Cardiac Fibrosis and Increased Blood Pressure
- A. Rickard, J. Morgan, G. Tesch, J. Funder, P. Fuller, M. Young
- Biology, MedicineHYPERTENSION
- 1 September 2009
It is shown that a novel and significant role is seen for macrophage signaling in the regulation of cardiac remodeling and systolic blood pressure in the deoxycorticosterone/salt model.
Transgenic Model of Aldosterone-Driven Cardiac Hypertrophy and Heart Failure
- Wenning Qin, A. Rudolph, E. Mcmahon
- Biology, MedicineCirculation Research
- 11 July 2003
The hypothesis that aldosterone blockade may provide additional therapeutic benefit in the treatment of heart failure is supported, as the deleterious consequences of inappropriate activation of cardiomyocyte mineralocorticoid receptors are confirmed and a tonic inhibitory role of glucocortioids is revealed in preventing such outcomes under physiological conditions.
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