title: Greater fractalkine expression in mesenteric arteries of female spontaneously hypertensive rats compared with males.
abstract: A mircoarray analysis was performed to identify novel inflammatory genes that are differentially expressed in the mesenteric arteries of male and female spontaneously hypertensive rats (SHRs). Fractalkine was found to be the inflammatory gene with the greatest differential expression in mesenteric arteries, with the expression being greater in female SHRs compared with males. Greater inflammatory mediators in female SHRs were verified by measuring urinary monocyte chemoattractant protein-1, transforming growth factor-beta, and tumor necrosis factor-alpha (TNF-alpha) excretion, all of which were greater in female SHRs compared with males. Real-time PCR, Western blot analysis, and ELISA verified greater soluble fractalkine in mesenteric arteries of female SHRs. Consistent with increased fractalkine expression, TNF-alpha-converting enzyme and TNF-alpha levels in mesenteric arteries were also greater in female SHRs. We next tested the hypothesis that mesenteric arteries from female SHRs will have greater fractalkine-induced dysfunction. Acetylcholine, sodium nitroprusside, phenylephrine, and KCl concentration-response curves were performed in third-order mesenteric arteries from male and female SHRs pretreated with either vehicle or fractalkine (1 microg/ml). Fractalkine decreased sensitivity to 1) acetylcholine in arteries from male SHRs, 2) phenylephrine in arteries from both sexes, and 3) KCl in arteries from female SHRs. In conclusion, urinary and vascular markers of inflammation are greater in female SHRs compared with males, although blood pressure and cardiovascular risk are less in females.
authors.affiliation: Vascular Biology Center, Medical College of Biotechnology and Genome Medicine, Medical College of Georgia, Austa, George, USA. sullivan@mail.mcg.edu
authors.forename: Jennifer C
authors.initials: JC
authors.lastname: Sullivan
authors.forename: Jennifer L
authors.initials: JL
authors.lastname: Pardieck
authors.forename: Derek
authors.initials: D
authors.lastname: Doran
authors.forename: Yan
authors.initials: Y
authors.lastname: Zhang
authors.forename: Jin-Xiong
authors.initials: JX
authors.lastname: She
authors.forename: Jennifer S
authors.initials: JS
authors.lastname: Pollock
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D018932:Chemokine CCL2 / Q000378:metabolism; D054428:Chemokine CX3CL1 / Q000378:metabolism*; D004195:Disease Models, Animal; D005260:Female; D006973:Hypertension / Q000378:metabolism*; D008297:Male; D008638:Mesenteric Arteries / Q000187:drug effects / Q000378:metabolism*; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D011918:Rats, Inbred SHR; D012727:Sex Characteristics; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014665:Vasodilator Agents / Q000494:pharmacology
chemical_list: C491766:Ccl2 protein, rat; D018932:Chemokine CCL2; D054428:Chemokine CX3CL1; D016212:Transforming Growth Factor beta; D014409:Tumor Necrosis Factor-alpha; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine; D011189:Potassium Chloride; D000109:Acetylcholine