| Transient receptor potential channels in rat renal microcirculation: actions of angiotensin II. | |
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MedLine Citation:
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PMID: 12110018 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: This study assessed the calcium-activating mechanisms mediating glomerular arteriolar constriction by angiotensin II (Ang II). METHODS: Immunohistochemical and physiological studies were carried out, using antibody against transient receptor potential (TRP)-1 and an isolated perfused kidney model. RESULTS: Immunohistochemical experiments demonstrated that TRP-1 proteins were transcribed on both afferent and efferent arteriolar myocytes. In the first series of physiological experiments, Ang II (0.3 nmol/L) considerably constricted afferent (20.2 +/- 0.9 to 14.9 +/- 0.7 microm) and efferent arterioles (18.4 +/- 0.7 to 14.0 +/- 0.7 microm). The addition of nifedipine (1 micromol/L) restored decrements in afferent (to 20.0 +/- 0.8 microm) but not efferent arteriolar diameters. Further administration of SKF-96365 (100 micromol/L), a TRP channel blocker, reversed efferent arteriolar constriction (to 16.2 +/- 0.8 micromol/L). In the second group, although 2-aminoethoxydiphenyl borate (100 micromol/L), an inhibitor of inositol trisphosphate-induced calcium release (IP3CR), did not alter glomerular arteriolar diameters, it prevented Ang II-induced afferent arteriolar constriction and attenuated efferent arteriolar constriction (18.8 +/- 0.8 to 16.9 +/- microm). Subsequent removal of extracellular calcium abolished residual efferent arteriolar constriction (to 19.1 +/- 0.8 microm). CONCLUSIONS: Our data provide evidence that Ang II elicits IP3CR, possibly inducing a cellular response that activates voltage-dependent calcium channels on afferent arterioles. The present results suggest that Ang II-induced efferent arteriolar constriction involves IP3CR and calcium influx sensitive to SKF-96365. |
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Authors:
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Tsuneo Takenaka; Hiromichi Suzuki; Hirokazu Okada; Tsutomu Inoue; Yoshihiko Kanno; Yuri Ozawa; Koichi Hayashi; Takao Saruta |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Kidney international Volume: 62 ISSN: 0085-2538 ISO Abbreviation: Kidney Int. Publication Date: 2002 Aug |
Date Detail:
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Created Date: 2002-07-11 Completed Date: 2003-01-13 Revised Date: 2012-02-07 |
Medline Journal Info:
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Nlm Unique ID: 0323470 Medline TA: Kidney Int Country: United States |
Other Details:
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Languages: eng Pagination: 558-65 Citation Subset: IM |
Affiliation:
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Department of Medicine, Saitama Medical College, Saitama, Japan. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Angiotensin II
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pharmacology* Animals Arterioles / drug effects, physiology Calcium / metabolism Calcium Channel Blockers / pharmacology Calcium Channels / physiology Imidazoles / pharmacology Ion Channel Gating / drug effects, physiology Kidney Glomerulus / blood supply Nifedipine / pharmacology Rats Rats, Sprague-Dawley Renal Circulation / drug effects*, physiology* Ryanodine / pharmacology TRPC Cation Channels Vasoconstrictor Agents / pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Calcium Channel Blockers; 0/Calcium Channels; 0/Imidazoles; 0/TRPC Cation Channels; 0/Vasoconstrictor Agents; 0/transient receptor potential cation channel, subfamily C, member 1; 11128-99-7/Angiotensin II; 130495-35-1/1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole; 15662-33-6/Ryanodine; 21829-25-4/Nifedipine; 7440-70-2/Calcium |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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