| Hypertension impairs postnatal vasculogenesis: role of antihypertensive agents. | |
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MedLine Citation:
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PMID: 18426993 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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We analyzed the effect of hypertension on postischemic vasculogenesis. Ischemia was induced by right femoral artery ligature in Wistar Kyoto rats (WKY) or spontaneously hypertensive rats (SHR) treated with or without angiotensin-converting enzyme inhibitor (Perindopril, 0.76 mg/kg/d) and angiotensin type 1 receptor blocker (losartan, 30 mg/kg/d). Basal postischemic neovascularization was reduced in SHR compared to WKY (P<0.05, n=8). Treatment with ACE inhibitor or angiotensin type 1 receptor blocker decreased blood pressure levels by 1.4- and 1.3-fold (P<0.001), respectively and restored vessel growth in SHR to WKY levels. Interestingly, 14 days after bone-marrow mononuclear cell (BM-MNC) transfusion, angiographic scores, capillary density, and foot perfusion were decreased by 1.4-, 1.5-, and 1.2-fold, respectively in SHR transfused with BM-MNCs isolated from SHR compared to those receiving BM-MNCs of WKY (P<0.05, n=6). Alteration in BM-MNCs proangiogenic potential was likely related to the reduction in their ability to mobilize into peripheral circulation, as revealed by the 2.9-fold decrease in number of circulating CD34+/CD117+ cells (P<0.001) and to differentiate into cells with endothelial phenotype, as revealed by the 2.1-fold reduction in percentages of DilLDL/BS-1 lectin positive cells (P<0.001). In addition, reactive oxygen species (ROS) levels were increased by 2.2-fold in SHR BM-MNCs compared to WKY BM-MNCs (P<0.01), as assessed by L-012 luminescence. Cotreatment with ACE inhibitor, angiotensin type 1 receptor blocker, or antioxidants (NAC 3 mmol/L, Apocynin 200 micromol/L) reduced ROS levels, improved the number of DilLDL/BS-1 lectin-positive cells by around 1.5-fold, and restored BM-MNCs proangiogenic effects in ischemic hindlimb. In conclusion, alteration in progenitor cell proangiogenic function may participate to the hypertension-induced impairment in postischemic revascularization. |
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Authors:
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Dong You; Clément Cochain; Céline Loinard; José Vilar; Barend Mees; Micheline Duriez; Bernard I Lévy; Jean-Sébastien Silvestre |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2008-04-21 |
Journal Detail:
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Title: Hypertension Volume: 51 ISSN: 1524-4563 ISO Abbreviation: Hypertension Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-05-23 Completed Date: 2008-06-30 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 7906255 Medline TA: Hypertension Country: United States |
Other Details:
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Languages: eng Pagination: 1537-44 Citation Subset: IM |
Affiliation:
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Cardiovascular Research Center INSERM U689 Lariboisière, Paris, France. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Antihypertensive Agents / pharmacology* Blood Pressure / drug effects, physiology Bone Marrow Cells / cytology, physiology Cell Differentiation / physiology Disease Models, Animal Endothelium, Vascular / cytology, physiology Hindlimb / blood supply Hydralazine / pharmacology Hypertension / drug therapy*, pathology, physiopathology* Ischemia / pathology, physiopathology Ligation Losartan / pharmacology Male Neovascularization, Physiologic / drug effects*, physiology* Oxidative Stress / drug effects, physiology Perindopril / pharmacology* Rats Rats, Inbred SHR Rats, Inbred WKY Stem Cells / cytology, physiology |
| Chemical | |
Reg. No./Substance:
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0/Antihypertensive Agents; 114798-26-4/Losartan; 82834-16-0/Perindopril; 86-54-4/Hydralazine |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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