Aldosterone and cardiovascular disease.
OBJECTIVE
The renin-angiotensin-aldosterone system is a co-ordinated hormonal cascade of major importance in the control of fluid and electrolyte homeostasis and blood pressure. During the past decade, the scientific community has realized that this system is also of paramount importance in pathophysiology of cardiovascular and renal target organ damage. In particular, inappropriately elevated aldosterone levels in the face of body sodium expansion have been incriminated in cardiac and vascular inflammation and fibrosis leading to remodeling and disease. Substantial advances on the role and mechanisms of aldosterone-induced tissue damage and novel findings on the genetic control of aldosterone secretion have been reported during the past year, and these are the subjects of this brief review.


RESULTS
A novel control mechanism for aldosterone secretion may be circadian clock genes, disruption of which leads to increased aldosterone secretion and hypertension. Animal models for human idiopathic hyperaldosteronism have been reported for the first time. Glucocorticoids have now been found to activate cardiac mineralocorticoid receptors during certain cardiovascular disease states. Crosstalk between mineralocorticoid and angiotensin AT1 receptors contributes to target organ damage. Endogenous cardiotonic steroids may explain at least some of the tissue damage during sodium loading previously attributed to aldosterone.


CONCLUSIONS
Insights on aldosterone and cardiovascular disease gained during the past year provide new avenues for research and applications for treatment in the future.
Carey
Robert M
RM
Division of Endocrinology and Metabolism, Department of Medicine, University of Virginia Health System, Charlottesville, Virginia 22908-1414, USA. rmc4c@virginia.edu
D000450:Aldosterone / Q000502:physiology*; D000818:Animals; D002318:Cardiovascular Diseases / Q000503:physiopathology*; D002940:Circadian Rhythm / Q000235:genetics; D004195:Disease Models, Animal; D006801:Humans; D006929:Hyperaldosteronism / Q000503:physiopathology*; D015221:Potassium Channels / Q000235:genetics / Q000502:physiology; D044140:Receptor, Angiotensin, Type 1 / Q000502:physiology; D018161:Receptors, Mineralocorticoid / Q000502:physiology
D015221:Potassium Channels; D044140:Receptor, Angiotensin, Type 1; D018161:Receptors, Mineralocorticoid; D000450:Aldosterone