Cyclooxygenase and thromboxane/prostaglandin receptor contribute to aortic endothelium-dependent dysfunction in aging female spontaneously hypertensive rats
Department of Kinesiology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada Submitted 18 June 2008 ; accepted in final form 17 August 2009 Cyclooxygenase (COX)-derived vasoconstrictory prostanoids contribute to impaired endothelium-dependent vasorelaxation in agi...
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| creator | Graham, Drew A Rush, James W. E |
| description | Department of Kinesiology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada
Submitted 18 June 2008
; accepted in final form 17 August 2009
Cyclooxygenase (COX)-derived vasoconstrictory prostanoids contribute to impaired endothelium-dependent vasorelaxation in aging male (m) spontaneously hypertensive rats (SHR); however, vasomotor responses in aging female (f) SHR and sex differences in aging SHR are unknown. Examining mechanisms governing dysfunction in aging fSHR will contribute to understanding sex-dependent vascular complications in advanced hypertension. Aortic endothelium-dependent relaxation dose responses (ACh) of 16- and 30-wk-old mSHR and fSHR and normotensive Wistar-Kyoto rats were examined in the absence (no drug control) and presence of COX inhibition [indomethacin (Indo)] and thromboxane/prostaglandin receptor inhibition (SQ-29548). No drug control-treated 16-wk mSHR exhibited considerable blunting of the peak relaxation response to ACh (e.g., 77 ± 4% relaxation to 10 –5 mol/l) vs. Wistar-Kyoto controls (89 ± 6%), and greater dysfunction occurred in 30-wk mSHR (63 ± 2%). Interestingly, ACh relaxations of fSHR were unimpaired at 16 wk (101 ± 2% to 10 –5 mol/l), but blunted in 30 wk (76 ± 4%). Indo and SQ-29548 restored robust ACh vasorelaxation in all groups (e.g., 113 ± 3 and 112 ± 3%, respectively, in Indo- and SQ-29548-treated 30-wk fSHR). Aortic COX-1 protein expression was elevated by 75% in 30-wk vs. 16-wk fSHR, whereas group-averaged ACh-stimulated aortic PGI 2 release (assessed as 6- keto-PGF 1 ) was 30% greater in 30-wk vs. 16-wk fSHR (9,926 ± 890 vs. 7,621 ± 690 pg·ml –1 ·mg dry wt –1 ), although this did not reach significance ( P = 0.0758). Dramatic deterioration of endothelium-dependent vasomotor function in fSHR across this age range involves COX and thromboxane/prostaglandin receptor, supporting a mechanism of impairment similar to that which occurs in aging mSHR.
endothelium-derived contracting factor; prostanoid; nitric oxide; sex difference; endothelium-dependent relaxation; prostaglandin I 2 ; thromboxane/prostaglandin receptor; SQ-29548
Address for reprint requests and other correspondence: J. W. E. Rush, Dept. of Kinesiology, Faculty of Applied Health Sciences, Univ. of Waterloo, 200 Univ. Ave. West, Waterloo, ON, Canada N2L 3G1 (e-mail: jwerush{at}uwaterloo.ca ). |
| doi_str_mv | 10.1152/japplphysiol.90785.2008 |
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Submitted 18 June 2008
; accepted in final form 17 August 2009
Cyclooxygenase (COX)-derived vasoconstrictory prostanoids contribute to impaired endothelium-dependent vasorelaxation in aging male (m) spontaneously hypertensive rats (SHR); however, vasomotor responses in aging female (f) SHR and sex differences in aging SHR are unknown. Examining mechanisms governing dysfunction in aging fSHR will contribute to understanding sex-dependent vascular complications in advanced hypertension. Aortic endothelium-dependent relaxation dose responses (ACh) of 16- and 30-wk-old mSHR and fSHR and normotensive Wistar-Kyoto rats were examined in the absence (no drug control) and presence of COX inhibition [indomethacin (Indo)] and thromboxane/prostaglandin receptor inhibition (SQ-29548). No drug control-treated 16-wk mSHR exhibited considerable blunting of the peak relaxation response to ACh (e.g., 77 ± 4% relaxation to 10 –5 mol/l) vs. Wistar-Kyoto controls (89 ± 6%), and greater dysfunction occurred in 30-wk mSHR (63 ± 2%). Interestingly, ACh relaxations of fSHR were unimpaired at 16 wk (101 ± 2% to 10 –5 mol/l), but blunted in 30 wk (76 ± 4%). Indo and SQ-29548 restored robust ACh vasorelaxation in all groups (e.g., 113 ± 3 and 112 ± 3%, respectively, in Indo- and SQ-29548-treated 30-wk fSHR). Aortic COX-1 protein expression was elevated by 75% in 30-wk vs. 16-wk fSHR, whereas group-averaged ACh-stimulated aortic PGI 2 release (assessed as 6- keto-PGF 1 ) was 30% greater in 30-wk vs. 16-wk fSHR (9,926 ± 890 vs. 7,621 ± 690 pg·ml –1 ·mg dry wt –1 ), although this did not reach significance ( P = 0.0758). Dramatic deterioration of endothelium-dependent vasomotor function in fSHR across this age range involves COX and thromboxane/prostaglandin receptor, supporting a mechanism of impairment similar to that which occurs in aging mSHR.
endothelium-derived contracting factor; prostanoid; nitric oxide; sex difference; endothelium-dependent relaxation; prostaglandin I 2 ; thromboxane/prostaglandin receptor; SQ-29548
Address for reprint requests and other correspondence: J. W. E. Rush, Dept. of Kinesiology, Faculty of Applied Health Sciences, Univ. of Waterloo, 200 Univ. Ave. West, Waterloo, ON, Canada N2L 3G1 (e-mail: jwerush{at}uwaterloo.ca ).</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/japplphysiol.90785.2008</identifier><identifier>PMID: 19696359</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Acetylcholine - pharmacology ; Age Factors ; Aging ; Animals ; Aorta - drug effects ; Aorta - enzymology ; Aorta - physiopathology ; Biological and medical sciences ; Blood Pressure ; Coronary vessels ; Cyclooxygenase 1 - metabolism ; Cyclooxygenase Inhibitors - pharmacology ; Disease Models, Animal ; Dose-Response Relationship, Drug ; Endothelium, Vascular - drug effects ; Endothelium, Vascular - enzymology ; Endothelium, Vascular - physiopathology ; Female ; Fundamental and applied biological sciences. Psychology ; Gender differences ; Hormones ; Hydrazines - pharmacology ; Hypertension ; Hypertension - enzymology ; Hypertension - physiopathology ; Indomethacin - pharmacology ; Male ; Membrane Proteins - antagonists & inhibitors ; Membrane Proteins - metabolism ; Phenylephrine - pharmacology ; Potassium Chloride - pharmacology ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; Receptors, Epoprostenol - antagonists & inhibitors ; Receptors, Epoprostenol - metabolism ; Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors ; Receptors, Thromboxane A2, Prostaglandin H2 - metabolism ; Rodents ; Sex Factors ; Vasoconstriction - drug effects ; Vasoconstrictor Agents - pharmacology ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>Journal of applied physiology (1985), 2009-10, Vol.107 (4), p.1059-1067</ispartof><rights>2009 INIST-CNRS</rights><rights>Copyright American Physiological Society Oct 2009</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c403t-4d469c7526d2bc231eb993fc28bed65085b9d65aec304207805d363f88039ad83</citedby><cites>FETCH-LOGICAL-c403t-4d469c7526d2bc231eb993fc28bed65085b9d65aec304207805d363f88039ad83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21997199$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19696359$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Graham, Drew A</creatorcontrib><creatorcontrib>Rush, James W. E</creatorcontrib><title>Cyclooxygenase and thromboxane/prostaglandin receptor contribute to aortic endothelium-dependent dysfunction in aging female spontaneously hypertensive rats</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Department of Kinesiology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada
Submitted 18 June 2008
; accepted in final form 17 August 2009
Cyclooxygenase (COX)-derived vasoconstrictory prostanoids contribute to impaired endothelium-dependent vasorelaxation in aging male (m) spontaneously hypertensive rats (SHR); however, vasomotor responses in aging female (f) SHR and sex differences in aging SHR are unknown. Examining mechanisms governing dysfunction in aging fSHR will contribute to understanding sex-dependent vascular complications in advanced hypertension. Aortic endothelium-dependent relaxation dose responses (ACh) of 16- and 30-wk-old mSHR and fSHR and normotensive Wistar-Kyoto rats were examined in the absence (no drug control) and presence of COX inhibition [indomethacin (Indo)] and thromboxane/prostaglandin receptor inhibition (SQ-29548). No drug control-treated 16-wk mSHR exhibited considerable blunting of the peak relaxation response to ACh (e.g., 77 ± 4% relaxation to 10 –5 mol/l) vs. Wistar-Kyoto controls (89 ± 6%), and greater dysfunction occurred in 30-wk mSHR (63 ± 2%). Interestingly, ACh relaxations of fSHR were unimpaired at 16 wk (101 ± 2% to 10 –5 mol/l), but blunted in 30 wk (76 ± 4%). Indo and SQ-29548 restored robust ACh vasorelaxation in all groups (e.g., 113 ± 3 and 112 ± 3%, respectively, in Indo- and SQ-29548-treated 30-wk fSHR). Aortic COX-1 protein expression was elevated by 75% in 30-wk vs. 16-wk fSHR, whereas group-averaged ACh-stimulated aortic PGI 2 release (assessed as 6- keto-PGF 1 ) was 30% greater in 30-wk vs. 16-wk fSHR (9,926 ± 890 vs. 7,621 ± 690 pg·ml –1 ·mg dry wt –1 ), although this did not reach significance ( P = 0.0758). Dramatic deterioration of endothelium-dependent vasomotor function in fSHR across this age range involves COX and thromboxane/prostaglandin receptor, supporting a mechanism of impairment similar to that which occurs in aging mSHR.
endothelium-derived contracting factor; prostanoid; nitric oxide; sex difference; endothelium-dependent relaxation; prostaglandin I 2 ; thromboxane/prostaglandin receptor; SQ-29548
Address for reprint requests and other correspondence: J. W. E. Rush, Dept. of Kinesiology, Faculty of Applied Health Sciences, Univ. of Waterloo, 200 Univ. Ave. West, Waterloo, ON, Canada N2L 3G1 (e-mail: jwerush{at}uwaterloo.ca ).</description><subject>Acetylcholine - pharmacology</subject><subject>Age Factors</subject><subject>Aging</subject><subject>Animals</subject><subject>Aorta - drug effects</subject><subject>Aorta - enzymology</subject><subject>Aorta - physiopathology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Coronary vessels</subject><subject>Cyclooxygenase 1 - metabolism</subject><subject>Cyclooxygenase Inhibitors - pharmacology</subject><subject>Disease Models, Animal</subject><subject>Dose-Response Relationship, Drug</subject><subject>Endothelium, Vascular - drug effects</subject><subject>Endothelium, Vascular - enzymology</subject><subject>Endothelium, Vascular - physiopathology</subject><subject>Female</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Gender differences</subject><subject>Hormones</subject><subject>Hydrazines - pharmacology</subject><subject>Hypertension</subject><subject>Hypertension - enzymology</subject><subject>Hypertension - physiopathology</subject><subject>Indomethacin - pharmacology</subject><subject>Male</subject><subject>Membrane Proteins - antagonists & inhibitors</subject><subject>Membrane Proteins - metabolism</subject><subject>Phenylephrine - pharmacology</subject><subject>Potassium Chloride - pharmacology</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>Receptors, Epoprostenol - antagonists & inhibitors</subject><subject>Receptors, Epoprostenol - metabolism</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</subject><subject>Receptors, Thromboxane A2, Prostaglandin H2 - metabolism</subject><subject>Rodents</subject><subject>Sex Factors</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasoconstrictor Agents - pharmacology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkduOFCEQhjtG486uvoISE7Pxomc59AEuzcRTsok3ek1ourqbCQ0t0Lr9Lj6sjDNR4wVUgK_-KuovipcE7wmp6d1RLYtdpi0ab_cCt7zeU4z5o2KXX2lJGkweFzve1rhsa95eFdcxHjEmVVWTp8UVEY1oWC12xc_Dpq33D9sITkVAyvUoTcHPnX9QDu6W4GNSo833xqEAGpbkA9LepWC6NQFKHikfktEIXO_TBNasc9nDko_gEuq3OKxOJ-MdyhJqNG5EA8zKAopL1sll_BrthqZtgZDARfMdUFApPiueDMpGeH6JN8XX9---HD6W958_fDq8vS91hVkqq75qhG5r2vS005QR6IRgg6a8g76pMa87kaMCzXBF87Bw3bOGDZxjJlTP2U1xe9bNv_22QkxyNlGDtefWZMsqzDnDTSZf_Uce_Rpcbk5SSknTYIoz1J4hnYcXAwxyCWZWYZMEy5N98l_75G_75Mm-nPniIr92M_R_8y5-ZeD1BVBRKzsE5bSJfzhKhGjzytybMzeZcfphAshLNT9up-q5k1ZWec-avwDJzLra</recordid><startdate>20091001</startdate><enddate>20091001</enddate><creator>Graham, Drew A</creator><creator>Rush, James W. E</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TS</scope><scope>7U7</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>P64</scope><scope>7X8</scope></search><sort><creationdate>20091001</creationdate><title>Cyclooxygenase and thromboxane/prostaglandin receptor contribute to aortic endothelium-dependent dysfunction in aging female spontaneously hypertensive rats</title><author>Graham, Drew A ; Rush, James W. E</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c403t-4d469c7526d2bc231eb993fc28bed65085b9d65aec304207805d363f88039ad83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Age Factors</topic><topic>Aging</topic><topic>Animals</topic><topic>Aorta - drug effects</topic><topic>Aorta - enzymology</topic><topic>Aorta - physiopathology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Coronary vessels</topic><topic>Cyclooxygenase 1 - metabolism</topic><topic>Cyclooxygenase Inhibitors - pharmacology</topic><topic>Disease Models, Animal</topic><topic>Dose-Response Relationship, Drug</topic><topic>Endothelium, Vascular - drug effects</topic><topic>Endothelium, Vascular - enzymology</topic><topic>Endothelium, Vascular - physiopathology</topic><topic>Female</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Gender differences</topic><topic>Hormones</topic><topic>Hydrazines - pharmacology</topic><topic>Hypertension</topic><topic>Hypertension - enzymology</topic><topic>Hypertension - physiopathology</topic><topic>Indomethacin - pharmacology</topic><topic>Male</topic><topic>Membrane Proteins - antagonists & inhibitors</topic><topic>Membrane Proteins - metabolism</topic><topic>Phenylephrine - pharmacology</topic><topic>Potassium Chloride - pharmacology</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>Receptors, Epoprostenol - antagonists & inhibitors</topic><topic>Receptors, Epoprostenol - metabolism</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors</topic><topic>Receptors, Thromboxane A2, Prostaglandin H2 - metabolism</topic><topic>Rodents</topic><topic>Sex Factors</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasoconstrictor Agents - pharmacology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Graham, Drew A</creatorcontrib><creatorcontrib>Rush, James W. E</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Physical Education Index</collection><collection>Toxicology Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Graham, Drew A</au><au>Rush, James W. E</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cyclooxygenase and thromboxane/prostaglandin receptor contribute to aortic endothelium-dependent dysfunction in aging female spontaneously hypertensive rats</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>2009-10-01</date><risdate>2009</risdate><volume>107</volume><issue>4</issue><spage>1059</spage><epage>1067</epage><pages>1059-1067</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Department of Kinesiology, Faculty of Applied Health Sciences, University of Waterloo, Waterloo, Ontario, Canada
Submitted 18 June 2008
; accepted in final form 17 August 2009
Cyclooxygenase (COX)-derived vasoconstrictory prostanoids contribute to impaired endothelium-dependent vasorelaxation in aging male (m) spontaneously hypertensive rats (SHR); however, vasomotor responses in aging female (f) SHR and sex differences in aging SHR are unknown. Examining mechanisms governing dysfunction in aging fSHR will contribute to understanding sex-dependent vascular complications in advanced hypertension. Aortic endothelium-dependent relaxation dose responses (ACh) of 16- and 30-wk-old mSHR and fSHR and normotensive Wistar-Kyoto rats were examined in the absence (no drug control) and presence of COX inhibition [indomethacin (Indo)] and thromboxane/prostaglandin receptor inhibition (SQ-29548). No drug control-treated 16-wk mSHR exhibited considerable blunting of the peak relaxation response to ACh (e.g., 77 ± 4% relaxation to 10 –5 mol/l) vs. Wistar-Kyoto controls (89 ± 6%), and greater dysfunction occurred in 30-wk mSHR (63 ± 2%). Interestingly, ACh relaxations of fSHR were unimpaired at 16 wk (101 ± 2% to 10 –5 mol/l), but blunted in 30 wk (76 ± 4%). Indo and SQ-29548 restored robust ACh vasorelaxation in all groups (e.g., 113 ± 3 and 112 ± 3%, respectively, in Indo- and SQ-29548-treated 30-wk fSHR). Aortic COX-1 protein expression was elevated by 75% in 30-wk vs. 16-wk fSHR, whereas group-averaged ACh-stimulated aortic PGI 2 release (assessed as 6- keto-PGF 1 ) was 30% greater in 30-wk vs. 16-wk fSHR (9,926 ± 890 vs. 7,621 ± 690 pg·ml –1 ·mg dry wt –1 ), although this did not reach significance ( P = 0.0758). Dramatic deterioration of endothelium-dependent vasomotor function in fSHR across this age range involves COX and thromboxane/prostaglandin receptor, supporting a mechanism of impairment similar to that which occurs in aging mSHR.
endothelium-derived contracting factor; prostanoid; nitric oxide; sex difference; endothelium-dependent relaxation; prostaglandin I 2 ; thromboxane/prostaglandin receptor; SQ-29548
Address for reprint requests and other correspondence: J. W. E. Rush, Dept. of Kinesiology, Faculty of Applied Health Sciences, Univ. of Waterloo, 200 Univ. Ave. West, Waterloo, ON, Canada N2L 3G1 (e-mail: jwerush{at}uwaterloo.ca ).</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>19696359</pmid><doi>10.1152/japplphysiol.90785.2008</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 8750-7587 |
| ispartof | Journal of applied physiology (1985), 2009-10, Vol.107 (4), p.1059-1067 |
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| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Age Factors Aging Animals Aorta - drug effects Aorta - enzymology Aorta - physiopathology Biological and medical sciences Blood Pressure Coronary vessels Cyclooxygenase 1 - metabolism Cyclooxygenase Inhibitors - pharmacology Disease Models, Animal Dose-Response Relationship, Drug Endothelium, Vascular - drug effects Endothelium, Vascular - enzymology Endothelium, Vascular - physiopathology Female Fundamental and applied biological sciences. Psychology Gender differences Hormones Hydrazines - pharmacology Hypertension Hypertension - enzymology Hypertension - physiopathology Indomethacin - pharmacology Male Membrane Proteins - antagonists & inhibitors Membrane Proteins - metabolism Phenylephrine - pharmacology Potassium Chloride - pharmacology Rats Rats, Inbred SHR Rats, Inbred WKY Receptors, Epoprostenol - antagonists & inhibitors Receptors, Epoprostenol - metabolism Receptors, Thromboxane A2, Prostaglandin H2 - antagonists & inhibitors Receptors, Thromboxane A2, Prostaglandin H2 - metabolism Rodents Sex Factors Vasoconstriction - drug effects Vasoconstrictor Agents - pharmacology Vasodilation - drug effects Vasodilator Agents - pharmacology |
| title | Cyclooxygenase and thromboxane/prostaglandin receptor contribute to aortic endothelium-dependent dysfunction in aging female spontaneously hypertensive rats |
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