Hypertension (HTN), and especially resistant HTN, is an endemic problem around the world with risk of end organ damage and increased rate of adverse effects despite treatment. Recent research has linked Aldosterone (Ald), the hormone responsible for sodium and water retention in the kidney, to resistant HTN in many cases. Aldosterone, part of the Renin-Angiotensin- Aldosterone System (RAAS), can be elevated beyond physiologic levels in many different disorders, and Primary Aldosteronism (PA) was recently shown to be the primary cause of secondary HTN. Further, Ald has known pleiotropic effects in other organ systems where there may be low levels of endogenous Ald production and functional mineralocorticoid receptors in the tissue. Specifically, Hyperaldosteronism (HA) has been linked to progression of chronic kidney disease, and pro-fibrotic, pro-inflammatory states in several different organ systems, especially the cardiovascular and hepatic systems. These effects by Ald on the renal, hepatic, cardiac, and vascular tissue suggest that novel treatment options for these patients. In cases where surgery is not viable to remove lesions creating the elevated levels of aldosterone, novel pharmacologic treatment should be explored, particularly targeting the Mineralocorticoid Receptor (MR) or Aldosterone Synthase (AS), which may be effective at preventing adverse outcomes in HTN patients, decreasing morbidity and mortality. This paper aims to explore in more depth the pathophysiologic role that hyperaldosteronism plays in HTN and future treatment options for such patients.
Authors: Taylor M. Stevens, Joy K. Saha, Yansheng Du
Keywords: aldosterone, hypertension, aldosteronism
DOI Number: not assigned Publication Year: 2018
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