{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,28]],"date-time":"2026-10-28T14:15:35Z","timestamp":1793196935249,"version":"4.5.0"},"reference-count":74,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2014,3,24]],"date-time":"2014-03-24T00:00:00Z","timestamp":1395619200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    The clinical manifestations of glucocorticoid excess include central obesity, hyperglycaemia, dyslipidaemia, electrolyte abnormalities and hypertension. A century on from Cushing's original case study, these cardinal features are prevalent in industrialized nations. Hypertension is the major modifiable risk factor for cardiovascular and renal disease and reflects underlying abnormalities of Na\n                    <jats:sup>+<\/jats:sup>\n                    homeostasis. Aldosterone is a master regulator of renal Na\n                    <jats:sup>+<\/jats:sup>\n                    transport but here we argue that glucocorticoids are also influential, particularly during moderate excess. The hypothalamic\u2013pituitary\u2013adrenal axis can affect renal Na\n                    <jats:sup>+<\/jats:sup>\n                    homeostasis on multiple levels, systemically by increasing mineralocorticoid synthesis and locally by actions on both the mineralocorticoid and glucocorticoid receptors, both of which are expressed in the kidney. The kidney also expresses both of the 11\u03b2\u2010hydroxysteroid dehydrogenase (11\u03b2HSD) enzymes. The intrarenal generation of active glucocorticoid by 11\u03b2HSD1 stimulates Na\n                    <jats:sup>+<\/jats:sup>\n                    reabsorption; failure to downregulate the enzyme during adaption to high dietary salt causes salt\u2010sensitive hypertension. The deactivation of glucocorticoid by 11\u03b2HSD2 underpins the regulatory dominance for Na\n                    <jats:sup>+<\/jats:sup>\n                    transport of mineralocorticoids and defines the \u2018aldosterone\u2010sensitive distal nephron\u2019. In summary, glucocorticoids can stimulate renal transport processes conventionally attributed to the renin\u2013angiotensin\u2013aldosterone system. Importantly, Na\n                    <jats:sup>+<\/jats:sup>\n                    and volume homeostasis do not exert negative feedback on the hypothalamic\u2013pituitary\u2013adrenal axis. These actions are therefore clinically relevant and may contribute to the pathogenesis of hypertension in conditions associated with elevated glucocorticoid levels, such as the metabolic syndrome and chronic stress.\n                  <\/jats:p>","DOI":"10.1113\/jphysiol.2013.267609","type":"journal-article","created":{"date-parts":[[2014,2,17]],"date-time":"2014-02-17T20:16:48Z","timestamp":1392668208000},"page":"1731-1744","source":"Crossref","is-referenced-by-count":85,"title":["Glucocorticoids and renal Na\n                    <sup>+<\/sup>\n                    transport: implications for hypertension and salt sensitivity"],"prefix":"10.1113","volume":"592","author":[{"given":"Robert W.","family":"Hunter","sequence":"first","affiliation":[{"name":"British Heart Foundation Centre for Cardiovascular Science University of Edinburgh Edinburgh UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jessica 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