{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,28]],"date-time":"2026-09-28T14:28:59Z","timestamp":1790605739635,"version":"4.1.0"},"reference-count":55,"publisher":"Wiley","issue":"9","license":[{"start":{"date-parts":[[2016,3,21]],"date-time":"2016-03-21T00:00:00Z","timestamp":1458518400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2016,5]]},"abstract":"<jats:sec><jats:title>Background and Purpose<\/jats:title><jats:p>Prostanoids derived from COX\u20102 and EP receptors are involved in vascular remodelling in different cardiovascular pathologies. This study evaluates the contribution of COX\u20102 and EP<jats:sub>1<\/jats:sub> receptors to vascular remodelling and function in hypertension.<\/jats:p><\/jats:sec><jats:sec><jats:title>Experimental Approach<\/jats:title><jats:p>Spontaneously hypertensive rats (SHR) and angiotensin II (AngII)\u2010infused (1.44 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup>, 2 weeks) mice were treated with the COX\u20102 inhibitor celecoxib (25 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> i.p) or with the EP<jats:sub>1<\/jats:sub> receptor antagonist SC19220 (10 mg\u00b7kg<jats:sup>\u22121<\/jats:sup>\u00b7day<jats:sup>\u22121<\/jats:sup> i.p.). COX\u20102<jats:sup>\u2212\/\u2212<\/jats:sup> mice with or without AngII infusion were also used.<\/jats:p><\/jats:sec><jats:sec><jats:title>Key Results<\/jats:title><jats:p>Celecoxib and SC19220 treatment did not modify the altered lumen diameter and wall : lumen ratio in mesenteric resistance arteries from SHR\u2010infused and\/or AngII\u2010infused animals. However, both treatments and COX\u20102 deficiency decreased the augmented vascular stiffness in vessels from hypertensive animals. This was accompanied by diminished vascular collagen deposition, normalization of altered elastin structure and decreased connective tissue growth factor and plasminogen activator inhibitor\u20101 gene expression. COX\u20102 deficiency and SC19220 treatment diminished the increased vasoconstrictor responses and endothelial dysfunction induced by AngII infusion. Hypertensive animals showed increased mPGES\u20101 expression and PGE<jats:sub>2<\/jats:sub> production in vascular tissue, normalized by celecoxib. Celecoxib treatment also decreased AngII\u2010induced macrophage infiltration and TNF\u2010\u03b1 expression. Macrophage conditioned media (MCM) increased COX\u20102 and collagen type I expression in vascular smooth muscle cells; the latter was reduced by celecoxib treatment.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions and Implications<\/jats:title><jats:p>COX\u20102 and EP<jats:sub>1<\/jats:sub> receptors participate in the increased extracellular matrix deposition and vascular stiffness, the impaired vascular function and inflammation in hypertension. Targeting PGE<jats:sub>2<\/jats:sub> receptors might have benefits in hypertension\u2010associated vascular damage.<\/jats:p><\/jats:sec>","DOI":"10.1111\/bph.13457","type":"journal-article","created":{"date-parts":[[2016,2,9]],"date-time":"2016-02-09T12:00:54Z","timestamp":1455019254000},"page":"1541-1555","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":56,"title":["Role of COX\u20102\u2010derived PGE<sub>2<\/sub> on vascular stiffness and function in hypertension"],"prefix":"10.1111","volume":"173","author":[{"given":"M S","family":"Avenda\u00f1o","sequence":"first","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S","family":"Mart\u00ednez\u2010Revelles","sequence":"additional","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"A","family":"Aguado","sequence":"additional","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M R","family":"Sim\u00f5es","sequence":"additional","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"},{"name":"Dept. Physiological Sciences Federal University of Espirito Santo  Vitoria Brazil"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M","family":"Gonz\u00e1lez\u2010Amor","sequence":"additional","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R","family":"Palacios","sequence":"additional","affiliation":[{"name":"Dept. Farmacolog\u00eda Universidad Aut\u00f3noma de Madrid (UAM), Instituto de Investigaci\u00f3n Hospital Universitario La Paz (IdiPAZ)  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P","family":"Guillem\u2010Llobat","sequence":"additional","affiliation":[{"name":"Centro de Biolog\u00eda Molecular \u201cSevero Ochoa\u201d UAM\u2010CSIC  Madrid Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"D V","family":"Vassallo","sequence":"additional","affiliation":[{"name":"Dept. 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