Source:http://linkedlifedata.com/resource/pubmed/id/12409978
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
5
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pubmed:dateCreated |
2002-10-31
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pubmed:abstractText |
The inhibitory effects of angiotensin-(1-7) on angiotensin II-induced vasoconstriction, growth of vascular smooth muscle cells, stimulation of protein kinase C, extracellular signal-regulated kinases (ERK), and angiotensin subtype 1 receptor (AT1) and subtype 2 receptor (AT2) mRNA expression were investigated. The hemodynamic effects of angiotensin-(1-7) were measured in Wistar rats. Vasoconstriction was measured using aortic rings. DNA synthesis or protein synthesis was measured in cultured vascular smooth muscle cells using [3H] thymidine or [3H] leucine incorporation, respectively. Angiotensin II stimulated protein kinase C and ERK1/2 were measured by Western blot analysis using phosphospecific protein kinase C and ERK1/2 antibodies. AT1 and AT2 receptor mRNA expression was measured using reverse-transcription polymerase chain reaction. Infusion of angiotensin II significantly increased whereas infusion of angiotensin-(1-7) had no effects on mean arterial blood pressure in Wistar rats. Angiotensin-(1-7) dose-dependently showed partial antagonism on angiotensin II-induced contraction of aortic rings. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced DNA synthesis and protein synthesis. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced activation of protein kinase C and ERK1/2. The administration of angiotensin-(1-7) showed partial antagonism on angiotensin II-induced downregulation of AT1 receptor mRNA expression, whereas AT2 receptor mRNA expression was unchanged. Angiotensin-(1-7) showed partial antagonism on angiotensin II-induced intracellular signal transduction and may play a crucial role in the adaptation process of AT1 receptors to sustained stimulation of angiotensin II.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin I,
http://linkedlifedata.com/resource/pubmed/chemical/Angiotensin II,
http://linkedlifedata.com/resource/pubmed/chemical/Antihypertensive Agents,
http://linkedlifedata.com/resource/pubmed/chemical/Mitogen-Activated Protein Kinases,
http://linkedlifedata.com/resource/pubmed/chemical/Peptide Fragments,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Angiotensin,
http://linkedlifedata.com/resource/pubmed/chemical/angiotensin I (1-7)
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pubmed:status |
MEDLINE
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pubmed:month |
Nov
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pubmed:issn |
0160-2446
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
40
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
693-700
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pubmed:dateRevised |
2009-11-19
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pubmed:meshHeading |
pubmed-meshheading:12409978-Angiotensin I,
pubmed-meshheading:12409978-Angiotensin II,
pubmed-meshheading:12409978-Animals,
pubmed-meshheading:12409978-Antihypertensive Agents,
pubmed-meshheading:12409978-Enzyme Activation,
pubmed-meshheading:12409978-Male,
pubmed-meshheading:12409978-Mitogen-Activated Protein Kinases,
pubmed-meshheading:12409978-Muscle, Smooth, Vascular,
pubmed-meshheading:12409978-Peptide Fragments,
pubmed-meshheading:12409978-Rats,
pubmed-meshheading:12409978-Rats, Wistar,
pubmed-meshheading:12409978-Receptors, Angiotensin,
pubmed-meshheading:12409978-Reverse Transcriptase Polymerase Chain Reaction,
pubmed-meshheading:12409978-Signal Transduction
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pubmed:year |
2002
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pubmed:articleTitle |
Angiotensin-(1-7) inhibits angiotensin II-induced signal transduction.
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pubmed:affiliation |
Department of Hypertension and Endocrinology, Daping Hospital, Third Military Medical University, Chongqing, Peoples Republic of China. zhuzm@cta.cq.cn
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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