Linked Life Data

18971538

Source:http://linkedlifedata.com/resource/pubmed/id/18971538

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
8
pubmed:dateCreated
2008-10-30
pubmed:abstractText
The present study aimed to examine the regulatory effect of hydrogen sulfide (H2S) on vascular collagen remodeling in hypertensive rats. After 5 weeks of H2S donor treatment, tail blood pressure, the endogenous H2S production rate, levels of hydroxyproline and collagen type I, collagen type I protein expression in the thoracic aorta, [3H]thymidine ([3H]TdR) incorporation, [3H]proline incorporation, and [3H]hydroxyproline secretion in cultured vascular smooth muscle cells (VSMCs) were measured. We also examined the effects of NaHS on angiotensin II-induced mitogen-activated protein kinase (MAPK) activation and angiotensin II type 1 (AT1) receptor binding affinity. Vascular hydroxyproline and collagen type I levels were high, and collagen type I immunohistochemical staining in the thoracic aorta was strong in SHRs compared to Wistar Kyoto (WKY) rats. [3H]TdR and [3H]proline incorporation and [3H]hydroxyproline secretion were also higher in cultured VSMCs from SHR than those from WKY rats. However, vascular H2S production was lower in SHR compared with WKY rats. Treatment with NaHS increased vascular H2S production in SHRs, and partly reversed the changes in [3H]TdR and [3H]proline incorporation and [3H]hydroxyproline secretion. In cultured VSMCs, [3H]TdR and [3H]proline incorporation stimulated by angiotensin II was inhibited by incubation with NaHS. The inhibitory effect of NaHS on VSMC proliferation and collagen generation was stronger in the SHR than in the WKY group. Moreover, NaHS could dose-dependently decrease angiotensin II-induced MAPK activation. NaHS also decreased AT1 receptor binding as well as the binding affinity of the AT1 receptor. Thus, in SHRs, which demonstrated vascular remodeling and collagen accumulation, the endogenous H2S pathway is involved in the regulation of excess vascular collagen.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0916-9636
pubmed:author
pubmed:issnType
Print
pubmed:volume
31
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1619-30
pubmed:meshHeading
pubmed-meshheading:18971538-Angiotensin II, pubmed-meshheading:18971538-Animals, pubmed-meshheading:18971538-Aorta, Thoracic, pubmed-meshheading:18971538-Blood Pressure, pubmed-meshheading:18971538-Cell Division, pubmed-meshheading:18971538-Collagen Type I, pubmed-meshheading:18971538-Hydrogen Sulfide, pubmed-meshheading:18971538-Hydroxyproline, pubmed-meshheading:18971538-Hypertension, pubmed-meshheading:18971538-MAP Kinase Signaling System, pubmed-meshheading:18971538-Male, pubmed-meshheading:18971538-Muscle, Smooth, Vascular, pubmed-meshheading:18971538-Proline, pubmed-meshheading:18971538-Rats, pubmed-meshheading:18971538-Rats, Inbred SHR, pubmed-meshheading:18971538-Rats, Inbred WKY, pubmed-meshheading:18971538-Receptor, Angiotensin, Type 1, pubmed-meshheading:18971538-Thymidine, pubmed-meshheading:18971538-Tritium, pubmed-meshheading:18971538-Vasoconstrictor Agents
pubmed:year
2008
pubmed:articleTitle
Regulatory effect of hydrogen sulfide on vascular collagen content in spontaneously hypertensive rats.
pubmed:affiliation
Department of Pediatrics, Peking University First Hospital, Beijing, PR China.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't