{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T15:49:53Z","timestamp":1761580193246},"reference-count":32,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2004,4]]},"abstract":"<jats:p> The present study tested the hypothesis that there is impaired function of \u03b1<jats:sub>2<\/jats:sub>-adrenergic autoreceptors and increased transmitter release from sympathetic nerves associated with mesenteric arteries and veins from DOCA-salt rats. High-performance liquid chromatography was used to measure the overflow of ATP and norepinephrine (NE) from electrically stimulated mesenteric artery and vein preparations in vitro. In sham arteries, nerve stimulation evoked a 1.5-fold increase in NE release, whereas in DOCA-salt arteries there was a 3.9-fold increase in NE release over basal levels ( P &lt; 0.05). In contrast, stimulated ATP release was not different in DOCA-salt arteries compared with sham arteries. In sham veins, nerve stimulation evoked a 2.9-fold increase in NE release, whereas in DOCA-salt veins there was a 8.4-fold increase in NE release over basal levels ( P &lt; 0.05). In sham rats NE release, normalized to basal levels, was greater in veins than in arteries ( P &lt; 0.05). The \u03b1<jats:sub>2<\/jats:sub>-adrenergic receptor antagonist yohimbine (1 \u03bcM) increased ATP and NE release in sham but not DOCA-salt arteries. The \u03b1<jats:sub>2<\/jats:sub>-adrenergic receptor agonist UK-14,304 (10 \u03bcM) decreased ATP release in sham but not DOCA-salt arteries. In sham veins, UK-14,304 decreased, but yohimbine increased, NE release; effects that were not observed in DOCA-salt veins. These data show that nerve stimulation causes a greater increase in NE release from nerves associated with veins compared with arteries. In addition, impairment of \u03b1<jats:sub>2<\/jats:sub>-adrenergic autoreceptor function in sympathetic nerves associated with arteries and veins from DOCA-salt rats results in increased NE release. <\/jats:p>","DOI":"10.1152\/ajpheart.00592.2003","type":"journal-article","created":{"date-parts":[[2004,3,12]],"date-time":"2004-03-12T13:52:56Z","timestamp":1079099576000},"page":"H1558-H1564","source":"Crossref","is-referenced-by-count":16,"title":["Impaired function of \u03b1<sub>2<\/sub>-adrenergic autoreceptors on sympathetic nerves associated with mesenteric arteries and veins in DOCA-salt hypertension"],"prefix":"10.1152","volume":"286","author":[{"given":"Min","family":"Luo","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Michigan 48824"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Gregory D.","family":"Fink","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Michigan 48824"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Keith J.","family":"Lookingland","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Michigan 48824"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"John A.","family":"Morris","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Michigan 48824"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James J.","family":"Galligan","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology and the Neuroscience Program, Michigan State University, East Lansing, Michigan 48824"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","reference":[{"key":"REF1","doi-asserted-by":"publisher","DOI":"10.1046\/j.1440-1681.2001.03460.x"},{"key":"REF2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2680.2001.00207.x"},{"key":"REF3","doi-asserted-by":"publisher","DOI":"10.1161\/01.HYP.25.6.1224"},{"key":"REF4","doi-asserted-by":"publisher","DOI":"10.1152\/ajpheart.1999.276.4.H1263"},{"key":"REF5","doi-asserted-by":"publisher","DOI":"10.1042\/cs0680089"},{"key":"REF6","unstructured":"Cassis LA, Stitzel RE, and Head RJ. 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