{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,29]],"date-time":"2026-04-29T13:08:19Z","timestamp":1777468099354,"version":"3.51.4"},"reference-count":53,"publisher":"American Physiological Society","issue":"2","funder":[{"DOI":"10.13039\/100000050","name":"HHS | NIH | National Heart, Lung, and Blood Institute (NHBLI)","doi-asserted-by":"publisher","award":["HL-080402"],"award-info":[{"award-number":["HL-080402"]}],"id":[{"id":"10.13039\/100000050","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Regulatory, Integrative and Comparative Physiology"],"published-print":{"date-parts":[[2015,7,15]]},"abstract":"<jats:p>Testosterone (TES) and other androgens exert a direct vasorelaxing action on the vasculature in vitro that is structurally specific and independent of cytosolic androgen receptor (AR). The effects of intravenous androgen infusions on mean arterial blood pressure (BP) and heart rate (HR) were determined in conscious, unrestrained, chronically catheterized, ganglionically blocked (hexamethonium, HEX; 30 mg\/kg ip) male Sprague-Dawley (SD) and testicular-feminized male (Tfm; AR-deficient) rats, 16\u201320 wk of age. BP and HR were recorded at baseline and with increasing doses of androgens (0.375\u20136.00 \u03bcmol\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>iv; 10 min\/dose). Data are expressed as means \u00b1 SE ( n = 5\u20138 rats\/group). In SD rats, baseline BP and HR averaged 103 \u00b1 4 mmHg and 353 \u00b1 12 beats\/min (bpm). TES produced a dose-dependent reduction in BP to a low of 87 \u00b1 4 mmHg (\u039416%), while HR was unchanged (354 \u00b1 14 bpm). Neither BP (109 \u00b1 3 mmHg) nor HR (395 \u00b1 13 bpm) were altered by vehicle (10% EtOH in 0.9% saline; 0.15 ml\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>, iv). In Tfm, TES produced a similar reduction in BP (99 \u00b1 3 to 86 \u00b1 3 mmHg, \u039413%); HR was unchanged (369 \u00b1 18 bpm). In SD, 5\u03b2-dihydrotestosterone (genomically inactive metabolite) produced a greater reduction in BP than TES (102 \u00b1 2 to 79 \u00b1 2 mmHg, \u039423%); HR was unchanged (361 \u00b1 9). A 20-\u03bcg iv bolus of sodium nitroprusside in both SD and Tfm rats reduced BP 30\u201340 mmHg, while HR was unchanged, confirming blockade by HEX. Pretreatment of SD rats with neuronal nitric oxide synthase (nNOS) inhibitor (S-methyl-thiocitrulline, SMTC; 20 \u03bcg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7min<jats:sup>\u22121<\/jats:sup>\u00d7 30 min) abolished the hypotensive effects of TES infusion on BP (104 \u00b1 2 vs. 101 \u00b1 2 mmHg) and HR (326 \u00b1 11 vs. 324 \u00b1 8 bpm). These data suggest the systemic hypotensive effect of TES and other androgens involves a direct vasodilatory action on the peripheral vasculature which, like the effect observed in isolated arteries, is structurally specific and AR-independent, and involves activation of nNOS.<\/jats:p>","DOI":"10.1152\/ajpregu.00110.2015","type":"journal-article","created":{"date-parts":[[2015,5,7]],"date-time":"2015-05-07T02:22:22Z","timestamp":1430965342000},"page":"R189-R195","source":"Crossref","is-referenced-by-count":25,"title":["Systemic hypotensive effects of testosterone are androgen structure-specific and neuronal nitric oxide synthase-dependent"],"prefix":"10.1152","volume":"309","author":[{"given":"Mercedes","family":"Perusqu\u00eda","sequence":"first","affiliation":[{"name":"Departamento de Biolog\u00eda Celular y Fisiolog\u00eda, Instituto de Investigaciones Biom\u00e9dicas, Universidad Nacional Aut\u00f3noma de M\u00e9xico, M\u00e9xico City, M\u00e9xico;"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Clayton D.","family":"Greenway","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology and Pharmacology, Texas A&amp;M University, College Station, Texas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Lisa M.","family":"Perkins","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology and Pharmacology, Texas A&amp;M University, College Station, Texas; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John N.","family":"Stallone","sequence":"additional","affiliation":[{"name":"Department of Veterinary Physiology and Pharmacology, Texas A&amp;M University, College Station, Texas; and"},{"name":"Women's Health Division, Michael E. 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