Under normal settings, adrenocorticotropic hormone can promote aldosterone production rapidly and transiently, albeit to a smaller amount than angiotensin II and potassium. Furthermore, ACTH promotes the synthesis of aldosterone both abruptly and chronically. Abrupt increases in ACTH levels such as those seen in patients with Cushing's syndrome will result in increased aldosterone production and secretion. Chronic increases in ACTH lead to increased aldosterone production by the adrenal cortex. This effect is mediated through the activation of transcription factors called nuclear receptors that regulate the expression of genes involved in aldosterone production and secretion. Activation of these receptors leads to increased activity of enzymes required for aldosterone production including steroid sulfotransferases, UDP-glucuronosyltransferases, and 17α-hydroxylase/C17,20-lyase. These enzymes are responsible for converting inactive precursors into active forms of aldosterone. Thus, chronic ACTH stimulation results in increased aldosterone production due to increased mRNA transcription and protein translation of these enzymes. A study conducted by Zuckerman et al. (2001) examined the effects of acute and chronic administration of ACTH on aldosterone production in rats. They found that acute injection of ACTH significantly increased plasma aldosterone concentrations within 30 minutes and this increase remained elevated for 3 hours after injection.