دورية أكاديمية

Reduced endothelium-dependent relaxation to anandamide in mesenteric arteries from young obese Zucker rats.

التفاصيل البيبلوغرافية
العنوان: Reduced endothelium-dependent relaxation to anandamide in mesenteric arteries from young obese Zucker rats.
المؤلفون: Lobato NS; Department of Biological Sciences, Federal University of Goias, Jatai, GO, Brazil., Filgueira FP, Prakash R, Giachini FR, Ergul A, Carvalho MH, Webb RC, Tostes RC, Fortes ZB
المصدر: PloS one [PLoS One] 2013 May 07; Vol. 8 (5), pp. e63449. Date of Electronic Publication: 2013 May 07 (Print Publication: 2013).
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; 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: Electronic-Print 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: Arachidonic Acids/*pharmacology , Endocannabinoids/*pharmacology , Endothelium, Vascular/*physiopathology , Mesenteric Arteries/*physiopathology , Obesity/*physiopathology , Polyunsaturated Alkamides/*pharmacology , Vasodilation/*drug effects, Acetyl-CoA Carboxylase/metabolism ; Adenylate Kinase/metabolism ; Animals ; Cannabinoid Receptor Agonists/pharmacology ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/enzymology ; In Vitro Techniques ; Male ; Mesenteric Arteries/drug effects ; Mesenteric Arteries/enzymology ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type III/metabolism ; Obesity/metabolism ; Phosphorylation/drug effects ; Protein Transport/drug effects ; Rats ; Rats, Zucker ; Receptor, Cannabinoid, CB1/metabolism ; Receptor, Cannabinoid, CB2/metabolism ; TRPV Cation Channels/metabolism
مستخلص: Impaired vascular function, manifested by an altered ability of the endothelium to release endothelium-derived relaxing factors and endothelium-derived contracting factors, is consistently reported in obesity. Considering that the endothelium plays a major role in the relaxant response to the cannabinoid agonist anandamide, the present study tested the hypothesis that vascular relaxation to anandamide is decreased in obese rats. Mechanisms contributing to decreased anandamide-induced vasodilation were determined. Resistance mesenteric arteries from young obese Zucker rats (OZRs) and their lean counterparts (LZRs) were used. Vascular reactivity was evaluated in a myograph for isometric tension recording. Protein expression and localization were analyzed by Western blotting and immunofluorescence, respectively. Vasorelaxation to anandamide, acetylcholine, and sodium nitroprusside, as well as to CB1, CB2, and TRPV1 agonists was decreased in endothelium-intact mesenteric arteries from OZRs. Incubation with an AMP-dependent protein kinase (AMPK) activator or a fatty acid amide hydrolase inhibitor restored anandamide-induced vascular relaxation in OZRs. CB1 and CB2 receptors protein expression was decreased in arteries from OZRs. Incubation of mesenteric arteries with anandamide evoked endothelial nitric oxide synthase (eNOS), AMPK and acetyl CoA carboxylase phosphorylation in LZRs, whereas it decreased phosphorylation of these proteins in OZRs. In conclusion, obesity decreases anandamide-induced relaxation in resistance arteries. Decreased cannabinoid receptors expression, increased anandamide degradation, decreased AMPK/eNOS activity as well as impairment of the response mediated by TRPV1 activation seem to contribute to reduce responses to cannabinoid agonists in obesity.
References: J Clin Invest. 1997 Sep 15;100(6):1538-46. (PMID: 9294122)
JAMA. 2002 Oct 9;288(14):1723-7. (PMID: 12365955)
Pharmacol Rev. 1991 Jun;43(2):143-201. (PMID: 1852779)
Nat Rev Drug Discov. 2008 May;7(5):438-55. (PMID: 18446159)
J Clin Invest. 2003 Aug;112(3):423-31. (PMID: 12897210)
Eur J Pharmacol. 2003 Sep 12;477(2):143-52. (PMID: 14519418)
Neuropharmacology. 2008 Jan;54(1):1-7. (PMID: 17631919)
Br J Pharmacol. 2009 Oct;158(4):1143-52. (PMID: 19702785)
Mol Cell Endocrinol. 2008 Apr 16;286(1-2 Suppl 1):S66-78. (PMID: 18343566)
Nature. 1999 Jul 29;400(6743):452-7. (PMID: 10440374)
Proc Natl Acad Sci U S A. 1991 Mar 15;88(6):2166-70. (PMID: 1848694)
Neurosci Lett. 1990 Mar 2;110(1-2):52-9. (PMID: 1691472)
Trends Pharmacol Sci. 2002 Apr;23(4):183-91. (PMID: 11931994)
Endocrinology. 1972 May;90(5):1320-30. (PMID: 5012744)
FEBS Lett. 1999 Jan 29;443(3):285-9. (PMID: 10025949)
Circulation. 2007 Sep 11;116(11 Suppl):I213-9. (PMID: 17846306)
Br J Pharmacol. 2007 Nov;152(5):717-24. (PMID: 17700721)
Circ Res. 2004 Nov 12;95(10):1027-34. (PMID: 15499026)
J Am Coll Cardiol. 2001 Dec;38(7):2048-54. (PMID: 11738314)
J Am Coll Cardiol. 2007 Aug 7;50(6):528-36. (PMID: 17678736)
Annu Rev Physiol. 2002;64:749-74. (PMID: 11826287)
Nature. 1996 Nov 7;384(6604):83-7. (PMID: 8900284)
Br J Pharmacol. 2007 Nov;152(5):699-708. (PMID: 17704831)
Circulation. 2004 Oct 5;110(14):1996-2002. (PMID: 15451779)
Nutr Metab Cardiovasc Dis. 2011 Oct;21(10):808-16. (PMID: 20554176)
Br J Pharmacol. 2001 Nov;134(5):1003-12. (PMID: 11682448)
Pathophysiology. 2008 Aug;15(2):79-89. (PMID: 18571908)
J Physiol. 2007 Jun 15;581(Pt 3):1163-71. (PMID: 17446219)
Br J Pharmacol. 2000 Aug;130(7):1483-8. (PMID: 10928948)
Circulation. 2005 Jan 25;111(3):363-8. (PMID: 15668353)
Curr Vasc Pharmacol. 2008 Oct;6(4):335-46. (PMID: 18855721)
J Neuroendocrinol. 2008 May;20 Suppl 1:58-62. (PMID: 18426501)
Nature. 1988 Sep 8;335(6186):164-7. (PMID: 2901042)
Nature. 1997 Oct 23;389(6653):816-24. (PMID: 9349813)
Atherosclerosis. 2008 Aug;199(2):248-56. (PMID: 18440538)
AAPS J. 2006 Apr 28;8(2):E298-306. (PMID: 16796380)
Br J Pharmacol. 2004 May;142(1):20-6. (PMID: 15131000)
J Pharmacol Exp Ther. 2000 Jul;294(1):27-32. (PMID: 10871291)
Crit Care Med. 2005 Nov;33(11):2629-36. (PMID: 16276190)
Nature. 1997 Dec 4;390(6659):518-21. (PMID: 9394002)
Am J Physiol Heart Circ Physiol. 2007 Oct;293(4):H2537-42. (PMID: 17693541)
Circ Res. 2009 Feb 27;104(4):496-505. (PMID: 19131647)
Diabetes. 2006 Nov;55(11):3053-60. (PMID: 17065342)
FASEB J. 1998 Aug;12(11):1035-44. (PMID: 9707176)
Br J Pharmacol. 2005 Oct;146(3):315-23. (PMID: 16025138)
J Biol Chem. 2005 Jul 1;280(26):25196-201. (PMID: 15899896)
Circ Res. 1977 Jul;41(1):19-26. (PMID: 862138)
J Neurosci. 2002 Jun 1;22(11):4720-7. (PMID: 12040079)
Hypertension. 2004 Aug;44(2):134-9. (PMID: 15249547)
PLoS One. 2007 Jul 25;2(7):e641. (PMID: 17653268)
Endocr Rev. 2006 Dec;27(7):750-61. (PMID: 17122359)
Br J Pharmacol. 2004 Jun;142(3):435-42. (PMID: 15148250)
Br J Pharmacol. 1992 Oct;107(2):544-52. (PMID: 1422598)
Diabetes. 2005 Oct;54(10):2838-43. (PMID: 16186383)
Hypertens Res. 2010 May;33(5):386-93. (PMID: 20442753)
J Am Coll Cardiol. 2003 May 21;41(10):1769-75. (PMID: 12767663)
Proc Natl Acad Sci U S A. 2009 Apr 14;106(15):6375-80. (PMID: 19307565)
Hypertension. 1999 Jan;33(1 Pt 2):429-34. (PMID: 9931142)
Am J Physiol. 1998 Jan;274(1):H375-81. (PMID: 9458889)
Int J Obes (Lond). 2007 Apr;31(4):692-9. (PMID: 17224929)
FASEB J. 2007 Feb;21(2):577-85. (PMID: 17167068)
معلومات مُعتمدة: P01 HL074167 United States HL NHLBI NIH HHS; R01 HL071138 United States HL NHLBI NIH HHS; HL71138 United States HL NHLBI NIH HHS; HL74167 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Arachidonic Acids)
0 (Cannabinoid Receptor Agonists)
0 (Endocannabinoids)
0 (Polyunsaturated Alkamides)
0 (Receptor, Cannabinoid, CB1)
0 (Receptor, Cannabinoid, CB2)
0 (TRPV Cation Channels)
31C4KY9ESH (Nitric Oxide)
EC 1.14.13.39 (Nitric Oxide Synthase Type III)
EC 2.7.4.3 (Adenylate Kinase)
EC 6.4.1.2 (Acetyl-CoA Carboxylase)
UR5G69TJKH (anandamide)
تواريخ الأحداث: Date Created: 20130514 Date Completed: 20131217 Latest Revision: 20211021
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC3646748
DOI: 10.1371/journal.pone.0063449
PMID: 23667622
قاعدة البيانات: MEDLINE
الوصف
تدمد:1932-6203
DOI:10.1371/journal.pone.0063449