{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,11,19]],"date-time":"2025-11-19T20:38:28Z","timestamp":1763584708966,"version":"3.40.5"},"reference-count":55,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2019,6,6]],"date-time":"2019-06-06T00:00:00Z","timestamp":1559779200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J of Clinical Hypertension"],"published-print":{"date-parts":[[2019,7]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Whether aldosterone itself contributes directly to macro\u2010 or microcirculatory disease in man or to adverse cardiovascular outcomes is not fully known. We report our long\u2010term single\u2010practice experience in 5 patients with chronic hyperaldosteronism (HA, including 3 with glucocorticoid remediable aldosteronism, GRA) treated with low\u2010dose amiloride (a specific epithelial sodium channel [ENaC] blocker) 5\u201010 (mean 7) mg daily for 14\u201028 (mean 20) years. Except for 1 GRA diagnosed in infancy, all had severe resistant hypertension. In each case, BP was normal or near\u2010normal within 1\u20104\u00a0weeks after starting amiloride and office BP\u2019s were well controlled for 20\u00a0years thereafter. Vascular studies and 24\u2010hour ambulatory BP monitoring with pulse wave analysis (cardiac output, vascular resistance, augmentation index, and reflection magnitude) were assessed after a mean of 18\u00a0years as were regional pulse wave velocities, pulse stiffening ratio, ankle\u2010brachial index, serum creatinine, estimated glomerular filtration rate, and spot urinary albumin:creatinine ratio. All indicators were completely normal in all patients after 18\u00a0years of amiloride, and none had a cardiovascular event during the 20\u2010year mean follow\u2010up. We conclude that long\u2010term ENaC blockade can normalize BP and protect macro\u2010 and microvascular function in patients with HA. This suggests that (a) any vasculopathic effects of aldosterone are mediated via ENaC, not MR activation itself, and are fully preventable or reversible with ENaC blockade or (b) aldosterone may not play a major BP\u2010independent role in human macro\u2010 and microcirculatory diseases. These and other widely divergent results in the literature underscore the need for additional studies regarding aldosterone, ENaC, and vascular disease.<\/jats:p>","DOI":"10.1111\/jch.13567","type":"journal-article","created":{"date-parts":[[2019,6,6]],"date-time":"2019-06-06T15:14:21Z","timestamp":1559834061000},"page":"922-928","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":7,"title":["Long\u2010term BP control and vascular health in patients with hyperaldosteronism treated with low\u2010dose, amiloride\u2010based therapy"],"prefix":"10.1111","volume":"21","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3570-8370","authenticated-orcid":false,"suffix":"Jr.","given":"Joseph L.","family":"Izzo","sequence":"first","affiliation":[{"name":"Department of Medicine, Jacobs School of Medicine University at Buffalo Buffalo New York"},{"name":"Erie County Medical Center Buffalo New 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