{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T23:19:48Z","timestamp":1791069588336,"version":"4.1.0"},"reference-count":30,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Hypertension"],"published-print":{"date-parts":[[2002,2]]},"abstract":"<jats:p>\n            Previous studies have established a role for 5-hydroxytryptamine (5-HT)\n            <jats:sub>2B<\/jats:sub>\n            and 5-HT\n            <jats:sub>1B<\/jats:sub>\n            receptors in mediating enhanced contraction to serotonin (5-HT) in arteries from hypertensive deoxycorticosterone acetate (DOCA)-salt rats. To determine whether the observed increase in responsiveness was due to upregulation of 5-HT receptors, we used Western analysis to measure 5-HT\n            <jats:sub>1B<\/jats:sub>\n            and 5-HT\n            <jats:sub>2B<\/jats:sub>\n            receptor protein density. In endothelium-denuded aortas from hypertensive DOCA-salt rats (mean systolic blood pressure 192\u00b16 mm Hg), 5-HT\n            <jats:sub>1B<\/jats:sub>\n            and 5-HT\n            <jats:sub>2B<\/jats:sub>\n            receptor proteins were upregulated \u22482-fold compared with the response in the aortas of sham-operated control rats (mean systolic blood pressure 119\u00b12 mm Hg). Contraction to 5-HT\n            <jats:sub>2B<\/jats:sub>\n            receptor agonists was also enhanced in arteries from Wistar-Furth rats given DOCA and salt. This strain is relatively resistant to the hypertensive effects of DOCA and salt treatment. A common factor between the model of DOCA-salt hypertension and the DOCA-salt\u2013treated Wistar-Furth rats is the presence of mineralocorticoids. Therefore, we tested the hypothesis that mineralocorticoids can upregulate 5-HT\n            <jats:sub>1B<\/jats:sub>\n            and 5-HT\n            <jats:sub>2B<\/jats:sub>\n            receptors. Aortas from normal Sprague-Dawley rats were incubated with aldosterone (100 nmol\/L) for 8, 12, 24, and 48 hours. The expression of 5-HT\n            <jats:sub>2B<\/jats:sub>\n            and 5-HT\n            <jats:sub>1B<\/jats:sub>\n            receptor proteins was significantly increased (\u22482- fold over vehicle treatment) by 8 hours. 5-HT\n            <jats:sub>2B<\/jats:sub>\n            and 5-HT\n            <jats:sub>1B<\/jats:sub>\n            receptors were upregulated by aldosterone in a concentration-dependent manner, and incubation with spironolactone (10 \u03bcmol\/L) blocked this upregulation. These data support the conclusion that the increased expression of 5-HT\n            <jats:sub>1B<\/jats:sub>\n            and 5-HT\n            <jats:sub>2B<\/jats:sub>\n            receptors observed in arteries from DOCA-salt rats may be partially due to mineralocorticoids acting via the mineralocorticoid receptor to modulate gene expression.\n          <\/jats:p>","DOI":"10.1161\/hy02t2.102793","type":"journal-article","created":{"date-parts":[[2002,7,28]],"date-time":"2002-07-28T23:16:47Z","timestamp":1027898207000},"page":"394-398","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":37,"title":["Upregulation of Arterial Serotonin 1B and 2B Receptors in Deoxycorticosterone Acetate-Salt Hypertension"],"prefix":"10.1161","volume":"39","author":[{"given":"Amy K.L.","family":"Banes","sequence":"first","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephanie W.","family":"Watts","sequence":"additional","affiliation":[{"name":"From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"1541","volume":"279","year":"1996","unstructured":"Watts SW. Serotonin activates the mitogen-activated protein kinase pathway in vascular smooth muscle: use of the mitogen-activated protein kinase kinase inhibitor PD098059. J Pharmacol Exp Ther. 1996; 279: 1541\u20131550.","journal-title":"J Pharmacol Exp Ther"},{"key":"e_1_3_2_2_2","first-page":"127","volume":"352","year":"1995","unstructured":"Yildiz O, Tuncer M. 5-HT1-like and 5-HT2A receptors mediate 5-hydroxytryptamine-induced contraction of rabbit isolated mesenteric artery. Naunyn Schmiedebergs Arch Pharmacol. 1995; 352: 127\u2013131.","journal-title":"Naunyn Schmiedebergs Arch Pharmacol"},{"key":"e_1_3_2_3_2","first-page":"1103","volume":"277","year":"1996","unstructured":"Watts SW, Baez M, Webb RC. The 5-hydroxytryptamine2B receptor and the 5-HT receptor signal transduction in mesenteric arteries from deoxycorticosterone acetate-salt hypertensive rats. J Pharmacol Exp Ther. 1996; 277: 1103\u20131113.","journal-title":"J Pharmacol Exp Ther"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.26.6.1056"},{"key":"e_1_3_2_5_2","first-page":"H944","year":"1999","unstructured":"Watts SW, Fink GD. 5-HT 2B-receptor antagonist LY272015 is antihypertensive in DOCA-salt hypertensive rats. Am J Physiol. 1999: H944\u2013H952.","journal-title":"Am J Physiol"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1161\/hyp.38.4.891"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0306-3623(99)00040-3"},{"key":"e_1_3_2_8_2","first-page":"682","volume":"22","year":"1996","unstructured":"Kayes K, Ziegler L, Yu CP, Brownie AC, Gallant S. The resistance of the Wistar\/Furth rat strain to steroid hypertension. Endocr Res. 1996; 22: 682\u2013689.","journal-title":"Endocr Res"},{"key":"e_1_3_2_9_2","first-page":"H1454","volume":"272","year":"1997","unstructured":"Ullian ME, Islam MM, Robinson CJ, Fitzgibbon WR, Tobin ET, Paul RV. Resistance to mineralocorticoids in Wistar-Furth rats. Am J Physiol. 1997; 272: H1454\u2013H1461.","journal-title":"Am J Physiol"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1161\/01.hyp.10.2.176"},{"key":"e_1_3_2_11_2","first-page":"H1167","volume":"265","year":"1993","unstructured":"Oguchi A, Ikeda U, Kanbe T, Tsuruya Y, Yamamoto K, Kawakami K, Medford RM, Shimada K. Regulation of Na-K-ATPase gene expression by aldosterone in vascular smooth muscle cells. 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