{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,17]],"date-time":"2026-03-17T14:15:25Z","timestamp":1773756925874,"version":"3.50.1"},"reference-count":22,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2000,11]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Hypertension is a  prominent feature of patients with Cushing\u2019s disease and ectopic  adrenocorticotropic hormone (ACTH) syndrome, who have elevated ACTH  levels. Chronic administration of ACTH (1-24) also raises blood  pressure in humans. This effect has been postulated to be due to  ACTH-induced increases in cortisol secretion in the adrenal gland. It  is well known that cortisol increases vascular tone by potentiating the  vasoconstrictor action of a number of pressor hormones. In the  present study, we show direct evidence that human aortic  endothelial cells possess the ACTH receptor.  11\u03b2-Dehydrogenation, converting cortisol to its inactive metabolite,  cortisone, mediated by vascular 11\u03b2-hydroxysteroid dehydrogenase type  2 is essential for the control of vascular tone, and the reduced  activity may be relevant to the pathogenesis of hypertension. We found  that ACTH (1-24) dose-dependently decreased the gene expression and  enzyme activity of 11\u03b2-hydroxysteroid dehydrogenase type 2 in these  cells, and the decrease was partially abolished by a selective ACTH  receptor antagonist. This may indicate that ACTH  potentiates the action of cortisol through its direct effect on the  vasculature. Therefore, the present study provides important  information for understanding the mechanism of ACTH-induced  hypertension.\n          <\/jats:p>","DOI":"10.1161\/01.hyp.36.5.862","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:25:31Z","timestamp":1339460731000},"page":"862-865","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":20,"title":["Functional Adrenocorticotropic Hormone Receptor in Cultured Human Vascular Endothelial Cells"],"prefix":"10.1161","volume":"36","author":[{"given":"Haruhiko","family":"Hatakeyama","sequence":"first","affiliation":[{"name":"From the Third Department of Internal Medicine, Fukui Medical University,  Fukui, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Satoru","family":"Inaba","sequence":"additional","affiliation":[{"name":"From the Third Department of Internal Medicine, Fukui Medical University,  Fukui, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Naomi","family":"Taniguchi","sequence":"additional","affiliation":[{"name":"From the Third Department of Internal Medicine, Fukui Medical University,  Fukui, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Isamu","family":"Miyamori","sequence":"additional","affiliation":[{"name":"From the Third Department of Internal Medicine, Fukui Medical University,  Fukui, Japan."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1126\/science.1325670"},{"key":"e_1_3_2_2_2","first-page":"2746","volume":"81","year":"1996","unstructured":"Stominski A, Ermark G, Martin M. ACTH receptor, CYP11A1, CYP17, and CYP21A2 genes are expressed in skin. J Clin Endocrinol Metab. 1996;81:2746\u20132749.","journal-title":"J Clin Endocrinol Metab"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1210\/endo.137.5.8612546"},{"key":"e_1_3_2_4_2","first-page":"501","volume":"5","year":"1983","unstructured":"Whitworth JA, Saines D, Thatcher R, Butkus A, Scoggins BA. Blood pressure and metabolic effects of ACTH in normotensive and hypertensive man. Clin Exp Hypertens. 1983;5:501\u2013522.","journal-title":"Clin Exp Hypertens"},{"key":"e_1_3_2_5_2","first-page":"795","volume":"6","year":"1984","unstructured":"Whitworth JA, Saines D, Scoggins BA. Blood pressure and metabolic effects of cortisol in man. Clin Exp Hypertens. 1984;6:795\u2013809.","journal-title":"Clin Exp Hypertens"},{"key":"e_1_3_2_6_2","first-page":"S34","volume":"37","year":"1992","unstructured":"Whitworth JA. Adrenocorticotrophin and steroid-induced hypertension in humans. Kidney Int Suppl. 1992;37:S34\u2013S37.","journal-title":"Kidney Int Suppl"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1097\/00004872-198907000-00005"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.10.6.608"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.19.6.567"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1007\/BF00637684"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.33.5.1179"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(18)55351-5"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1016\/0303-7207(95)03546-J"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.25.1.67"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.23.5.577"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0021-9258(19)51084-5"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1677\/joe.0.1480419"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1365-2265.1992.tb01478.x"},{"key":"e_1_3_2_19_2","first-page":"345","volume":"25","year":"1987","unstructured":"Eisenschmid B, Heilmann P, Oelkers W, Rejaibi R, Schoneshofer M. 20-Dihydroisomers of cortisol and cortisone in human urine: excretion rates under different physiological conditions. J Clin Chem Clin Biochem. 1987;25:345\u2013349.","journal-title":"J Clin Chem Clin Biochem"},{"key":"e_1_3_2_20_2","doi-asserted-by":"publisher","DOI":"10.1530\/eje.0.1340301"},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.31.1.459"},{"key":"e_1_3_2_22_2","doi-asserted-by":"publisher","DOI":"10.1111\/j.1440-1681.1987.tb00958.x"}],"container-title":["Hypertension"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ahajournals.org\/doi\/full\/10.1161\/01.HYP.36.5.862","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,5,12]],"date-time":"2024-05-12T17:31:22Z","timestamp":1715535082000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ahajournals.org\/doi\/10.1161\/01.HYP.36.5.862"}},"subtitle":["Possible Role in Control of Blood Pressure"],"short-title":[],"issued":{"date-parts":[[2000,11]]},"references-count":22,"journal-issue":{"issue":"5","published-print":{"date-parts":[[2000,11]]}},"alternative-id":["10.1161\/01.HYP.36.5.862"],"URL":"https:\/\/doi.org\/10.1161\/01.hyp.36.5.862","relation":{},"ISSN":["0194-911X","1524-4563"],"issn-type":[{"value":"0194-911X","type":"print"},{"value":"1524-4563","type":"electronic"}],"subject":[],"published":{"date-parts":[[2000,11]]},"assertion":[{"value":"2000-02-17","order":0,"name":"received","label":"Received","group":{"name":"publication_history","label":"Publication History"}},{"value":"2000-05-19","order":1,"name":"accepted","label":"Accepted","group":{"name":"publication_history","label":"Publication History"}},{"value":"2000-11-01","order":2,"name":"published","label":"Published","group":{"name":"publication_history","label":"Publication History"}}]}}