دورية أكاديمية
أعرض في EDS

Upregulation of ERK1/2-eNOS via AT2 receptors decreases the contractile response to angiotensin II in resistance mesenteric arteries from obese rats.

التفاصيل البيبلوغرافية
العنوان: Upregulation of ERK1/2-eNOS via AT2 receptors decreases the contractile response to angiotensin II in resistance mesenteric arteries from obese rats.
المؤلفون: Hagihara GN; Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Lobato NS; Department of Biological Sciences, Division of Cardiovascular Physiology, Federal University of Goias, Jatai, Brazil., Filgueira FP; Department of Biological Sciences, Division of Cardiovascular Physiology, Federal University of Goias, Jatai, Brazil., Akamine EH; Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Aragão DS; Department of Medicine, Division of Nephrology, Escola Paulista de Medicina, Federal University of Sao Paulo, Sao Paulo, Brazil., Casarini DE; Department of Medicine, Division of Nephrology, Escola Paulista de Medicina, Federal University of Sao Paulo, Sao Paulo, Brazil., Carvalho MH; Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil., Fortes ZB; Department of Pharmacology, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil.
المصدر: PloS one [PLoS One] 2014 Aug 29; Vol. 9 (8), pp. e106029. Date of Electronic Publication: 2014 Aug 29 (Print Publication: 2014).
نوع المنشور: Journal Article; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
أسماء مطبوعة: Original Publication: San Francisco, CA : Public Library of Science
مواضيع طبية MeSH: Mesenteric Arteries/*physiology , Mitogen-Activated Protein Kinase 1/*metabolism , Mitogen-Activated Protein Kinase 3/*metabolism , Nitric Oxide Synthase Type III/*metabolism , Obesity/*physiopathology , Receptor, Angiotensin, Type 2/*metabolism, Angiotensin II/pharmacology ; Angiotensin II Type 2 Receptor Blockers/pharmacology ; Animals ; Blotting, Western ; Endothelium, Vascular/physiology ; Enzyme Inhibitors/pharmacology ; Imidazoles/pharmacology ; In Vitro Techniques ; Male ; Mesenteric Arteries/metabolism ; Mitogen-Activated Protein Kinase 1/antagonists & inhibitors ; Mitogen-Activated Protein Kinase 3/antagonists & inhibitors ; NG-Nitroarginine Methyl Ester/pharmacology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/antagonists & inhibitors ; Obesity/metabolism ; Phosphorylation/drug effects ; Pyridines/pharmacology ; Rats, Wistar ; Up-Regulation ; Vasoconstriction/drug effects ; Vasoconstrictor Agents/pharmacology
مستخلص: It has been clearly established that mitogen-activated protein kinases (MAPKS) are important mediators of angiotensin II (Ang II) signaling via AT1 receptors in the vasculature. However, evidence for a role of these kinases in changes of Ang II-induced vasoconstriction in obesity is still lacking. Here we sought to determine whether vascular MAPKs are differentially activated by Ang II in obese animals. The role of AT2 receptors was also evaluated. Male monosodium glutamate-induced obese (obese) and non-obese Wistar rats (control) were used. The circulating concentrations of Ang I and Ang II, determined by HPLC, were increased in obese rats. Ang II-induced isometric contraction was decreased in endothelium-intact resistance mesenteric arteries from obese compared with control rats and exhibited a retarded AT1 receptor antagonist response. Blocking of AT2 receptors and inhibition of either endothelial nitric oxide synthase (eNOS) or extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) restored Ang II-induced contraction in obese rats. Western blot analysis revealed increased protein expression of AT2 receptors in arteries from obese rats. Basal and Ang II-induced ERK1/2 phosphorylation was also increased in obese rats. Blockade of either AT1 or AT2 receptors corrected the increased ERK1/2 phosphorylation in arteries from obese rats to levels observed in control preparations. Phosphorylation of eNOS was increased in obese rats. Incubation with the ERK1/2 inhibitor before Ang II stimulation did not affect eNOS phosphorylation in control rats; however, it corrected the increased phosphorylation of eNOS in obese rats. These results clearly demonstrate that enhanced AT2 receptor and ERK1/2-induced, NO-mediated vasodilation reduces Ang II-induced contraction in an endothelium-dependent manner in obese rats.
References: Regul Pept. 2012 Oct 10;178(1-3):64-70. (PMID: 22749992)
Cell Signal. 1997 Aug;9(5):337-51. (PMID: 9376213)
Hypertension. 1999 Nov;34(5):1112-6. (PMID: 10567191)
Peptides. 2012 Oct;37(2):247-51. (PMID: 22902596)
J Hum Hypertens. 1999 Jan;13 Suppl 1:S11-20; discussion S33-4. (PMID: 10076916)
Eur J Pharmacol. 1987 Mar 3;135(1):61-8. (PMID: 3552708)
Hypertension. 2005 May;45(5):840-4. (PMID: 15738342)
Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2537-42. (PMID: 17693541)
J Biol Chem. 1998 Jun 12;273(24):15022-9. (PMID: 9614110)
Circ Res. 1977 Jul;41(1):19-26. (PMID: 862138)
Nature. 2002 Nov 21;420(6913):333-6. (PMID: 12447443)
J Mol Med (Berl). 2001;79(1):21-9. (PMID: 11327100)
J Clin Invest. 1999 Mar;103(6):789-97. (PMID: 10079099)
Mol Cell Endocrinol. 2009 Apr 29;302(2):148-58. (PMID: 19059306)
J Clin Invest. 1997 Jul 15;100(2):264-9. (PMID: 9218502)
Am J Physiol Heart Circ Physiol. 2007 Apr;292(4):H1722-7. (PMID: 17142345)
Pharmacol Rev. 1993 Jun;45(2):205-51. (PMID: 8372104)
Circ Res. 1998 Jan 9-23;82(1):7-12. (PMID: 9440699)
Am J Physiol Regul Integr Comp Physiol. 2008 Jul;295(1):R144-54. (PMID: 18463192)
Hypertension. 2005 Feb;45(2):270-5. (PMID: 15596573)
Physiol Genomics. 2000 Jan 24;2(1):13-20. (PMID: 11015577)
Biochem Biophys Res Commun. 1999 Aug 2;261(2):345-9. (PMID: 10425188)
Endocr Rev. 2003 Jun;24(3):261-71. (PMID: 12788798)
Am J Physiol Cell Physiol. 2007 Jan;292(1):C82-97. (PMID: 16870827)
Hypertension. 2000 Jan;35(1 Pt 2):329-36. (PMID: 10642320)
Hypertension. 1985 Mar-Apr;7(2):244-52. (PMID: 2984118)
Am J Physiol Endocrinol Metab. 2004 Jun;286(6):E891-5. (PMID: 14749209)
Nutr Metab Cardiovasc Dis. 2011 Oct;21(10):808-16. (PMID: 20554176)
Clin Sci (Lond). 2008 Mar;114(5):375-80. (PMID: 17953515)
Diabetes. 2005 Feb;54(2):402-11. (PMID: 15677498)
J Hypertens. 1999 Jul;17(7):907-16. (PMID: 10419063)
Circulation. 1999 Jan 26;99(3):392-9. (PMID: 9918526)
J Cardiovasc Pharmacol Ther. 2010 Mar;15(1):78-83. (PMID: 20075153)
Am J Physiol Heart Circ Physiol. 2000 Aug;279(2):H741-51. (PMID: 10924074)
Circulation. 2004 May 18;109(19):2296-301. (PMID: 15117835)
Curr Opin Nephrol Hypertens. 2007 Mar;16(2):122-8. (PMID: 17293687)
Hypertension. 1999 Jan;33(1 Pt 2):366-72. (PMID: 9931131)
Hypertension. 2010 Feb;55(2):207-13. (PMID: 20038757)
J Hypertens. 2004 Jun;22(6):1141-9. (PMID: 15167449)
Am J Physiol Cell Physiol. 2004 Aug;287(2):C494-9. (PMID: 15084475)
Biochem Biophys Res Commun. 1989 Nov 30;165(1):196-203. (PMID: 2590220)
Hypertension. 2005 May;45(5):967-73. (PMID: 15837834)
Hypertension. 2001 Jul;38(1):56-64. (PMID: 11463760)
Curr Clin Pharmacol. 2014 Feb;9(1):2-9. (PMID: 23270435)
N Engl J Med. 1981 Apr 16;304(16):930-3. (PMID: 7010165)
Diabetologia. 1985 Jul;28(7):412-9. (PMID: 3899825)
Regul Pept. 2005 May 15;128(1):43-50. (PMID: 15721486)
Mol Pharmacol. 1995 Oct;48(4):601-9. (PMID: 7476884)
المشرفين على المادة: 0 (Angiotensin II Type 2 Receptor Blockers)
0 (Enzyme Inhibitors)
0 (Imidazoles)
0 (Pyridines)
0 (Receptor, Angiotensin, Type 2)
0 (Vasoconstrictor Agents)
11128-99-7 (Angiotensin II)
130663-39-7 (PD 123319)
31C4KY9ESH (Nitric Oxide)
EC 1.14.13.39 (Nitric Oxide Synthase Type III)
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1)
EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
OU13V1EYWQ (SB 203580)
V55S2QJN2X (NG-Nitroarginine Methyl Ester)
تواريخ الأحداث: Date Created: 20140830 Date Completed: 20150626 Latest Revision: 20211021
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC4149482
DOI: 10.1371/journal.pone.0106029
PMID: 25170617
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0106029