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(Hypertension. 2007;50:31.)
© 2007 American Heart Association, Inc.

Editorial Commentary

Aldosterone

Villain or Protector?

Gail K. Adler; Gordon H. Williams

From the Cardiovascular Endocrinology Section, Division of Endocrinology, Diabetes, and Hypertension, Brigham and Women’s Hospital, Harvard Medical School, Boston, Mass.

Correspondence to Gordon H. Williams, MD, Cardiovascular Endocrinology Section, Division of Endocrinology, Diabetes and Hypertension, 221 Longwood Avenue, Boston, MA 02115. E-mail gwilliams@partners.org

An extract of the first 250 words of the full text is provided, because this article has no abstract.

During the past decade, there has been heightened interest in aldosterone as a cardiovascular risk factor, fueled by studies documenting its effects on tissues other than epithelial cells. Of particular interest is the role of aldosterone in exacerbating vascular injury. It is likely that the mechanisms mediating the vascular effects of aldosterone differ from its effects on epithelial cells, eg, the renal collecting tubule. For more than a quarter of a century, it also had been assumed that the primary mechanism of aldosterone was mediated by activation of the mineralocorticoid receptor (MR), which in turn increased transcription of MR-responsive genes.

Recently, it has been documented that aldosterone can produce rapid cellular responses—MR-mediated increases in phosphorylation of transduction factors, eg, extracellular signal regulated kinase 1 and 2 (ERK1/2), protein kinase C (PKC), and endothelial nitric oxide synthase (eNOS), and changes in intracellular calcium and hydrogen ions—in addition to its traditional genomic responses. Sometimes these rapid effects are called "nongenomic." However, it is likely that even the "rapid" actions of aldosterone can lead to genomic effects. Thus, we will use the terms "rapid" and "genomic" to contrast 2 major mechanisms of action of aldosterone.

These rapid effects may be beneficial or detrimental depending on the environment in which aldosterone is acting. For example, phosphorylation of eNOS in endothelial cells leading to increased NO production and vasodilation would likely be beneficial in an environment where there is decreased perfusion to a vital organ. Activation of vasoconstriction through increases in cytosolic calcium or phosphorylation . . . [Full Text of this Article]

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