{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,13]],"date-time":"2026-05-13T08:21:41Z","timestamp":1778660501023,"version":"3.51.4"},"reference-count":60,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2011,8]]},"abstract":"<jats:p>Uridine adenosine tetraphosphate (Up<jats:sub>4<\/jats:sub>A) was reported as a novel endothelium-derived contracting factor. Up<jats:sub>4<\/jats:sub>A contains both purine and pyrimidine moieties, which activate purinergic (P2)X and P2Y receptors. However, alterations in the vasoconstrictor responses to Up<jats:sub>4<\/jats:sub>A in hypertensive states remain unclear. The present study examined the effects of Up<jats:sub>4<\/jats:sub>A on contraction of isolated renal arteries (RA) and pulmonary arteries (PA) from DOCA-salt rats using isometric tension recording. RA from DOCA-salt rats exhibited increased contraction to Up<jats:sub>4<\/jats:sub>A versus arteries from control uninephrectomized rats in the absence and presence of N<jats:sup>G<\/jats:sup>-nitro-l-arginine (nitric oxide synthase inhibitor). On the other hand, the Up<jats:sub>4<\/jats:sub>A-induced contraction in PA was similar between the two groups. Up<jats:sub>4<\/jats:sub>A-induced contraction was inhibited by suramin (nonselective P2 antagonist) but not by diinosine pentaphosphate pentasodium salt hydrate (Ip<jats:sub>5<\/jats:sub>I; P2X<jats:sub>1<\/jats:sub>antagonist) in RA from both groups. Furthermore, 2-thiouridine 5\u2032-triphosphate tetrasodium salt (2-ThioUTP; P2Y<jats:sub>2<\/jats:sub>agonist)-, uridine-5\u2032-(\u03b3-thio)-triphosphate trisodium salt (UTP\u03b3S; P2Y<jats:sub>2<\/jats:sub>\/P2Y<jats:sub>4<\/jats:sub>agonist)-, and 5-iodouridine-5\u2032- O-diphosphate trisodium salt (MRS 2693; P2Y<jats:sub>6<\/jats:sub>agonist)-induced contractions were all increased in RA from DOCA-salt rats. Protein expression of P2Y<jats:sub>2<\/jats:sub>-, P2Y<jats:sub>4<\/jats:sub>-, and P2Y<jats:sub>6<\/jats:sub>receptors in RA was similar between the two groups. In DOCA-salt RA, the enhanced Up<jats:sub>4<\/jats:sub>A-induced contraction was reduced by PD98059, an ERK pathway inhibitor, and Up<jats:sub>4<\/jats:sub>A-stimulated ERK activation was increased. These data are the first to indicate that Up<jats:sub>4<\/jats:sub>A-induced contraction is enhanced in RA from DOCA-salt rats. Enhanced P2Y receptor signaling and activation of the ERK pathway together represent a likely mechanism mediating the enhanced Up<jats:sub>4<\/jats:sub>A-induced contraction. Up<jats:sub>4<\/jats:sub>A might be of relevance in the pathophysiology of vascular tone regulation and renal dysfunction in arterial hypertension.<\/jats:p>","DOI":"10.1152\/ajpheart.00084.2011","type":"journal-article","created":{"date-parts":[[2011,5,7]],"date-time":"2011-05-07T04:55:44Z","timestamp":1304744144000},"page":"H409-H417","source":"Crossref","is-referenced-by-count":32,"title":["Uridine adenosine tetraphosphate-induced contraction is increased in renal but not pulmonary arteries from DOCA-salt hypertensive rats"],"prefix":"10.1152","volume":"301","author":[{"given":"Takayuki","family":"Matsumoto","sequence":"first","affiliation":[{"name":"Department of Physiology, Georgia Health Sciences University, Augusta, Georgia;"},{"name":"Department of Physiology and Morphology, Institute of Medicinal Chemistry, Hoshi University, Shinagawa-ku, Tokyo, Japan; and"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Rita C.","family":"Tostes","sequence":"additional","affiliation":[{"name":"Department of Pharmacology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Sao Paulo, Brazil"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R. 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