You will be shown an abstract from a biomedical research paper. Given this abstract, your task is to extract all unique entities of the following types: ["Chemical"].

Please return the output as a JSON object of the format: {"Chemical": ["Arsenic", ...]}. The keys should be entity types and values should be lists of extracted entities belonging to the corresponding type. If you cannot find entities belonging to a specific type, the value should be [].

Only output the JSON object and do not include any additional text.

Abstract:

Genetics of mineralocorticoid excess: an update for clinicians. Aldosterone plays a major role in regulating sodium and potassium homeostasis, and blood pressure. More recently aldosterone has emerged as a key hormone in mediating end organ damage. In extreme cases, dysregulated aldosterone production leads to primary aldosteronism, the most common form of secondary hypertension. However, even within the physiological range, high levels of aldosterone are associated with an increased risk of developing hypertension over time. Primary aldosteronism represents the most common and curable form of hypertension, with a prevalence that increases with the severity of hypertension. Although genetic causes underlying glucocorticoid remediable aldosteronism, one of the three Mendelian forms of primary aldosteronism, were established some time ago, somatic and inherited mutations in the potassium channel GIRK4 have only recently been implicated in the formation of aldosterone producing adenoma and in familial hyperaldosteronism type 3. Moreover, recent findings have identified somatic mutations in two additional genes, involved in maintaining intracellular ionic homeostasis and cell membrane potential, in a subset of aldosterone producing adenoma.This review summarizes our current knowledge on the genetic determinants that contribute to variations in plasma aldosterone and renin levels in the general population, and the genetics of familial and sporadic primary aldosteronism. Various animal models that have significantly improved our understanding of the pathophysiology of excess aldosterone production will also be discussed. Finally, we will outline the cardiovascular, renal and metabolic consequences of mineralocorticoid excess beyond blood pressure regulation.
{"Chemical": ["Aldosterone", "potassium", "aldosterone", "sodium"]}