Adenine-induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling.
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| Title: | Adenine-induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling. |
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| Authors: | Nguy, L., Shubbar, E., Jernås, M., Nookaew, I., Lundgren, J., Olsson, B., Nilsson, H., Guron, G. |
| Source: | Acta Physiologica. Dec2016, Vol. 218 Issue 4, p250-264. 15p. |
| Subjects: | Treatment of chronic kidney failure, Protein expression, Vascular smooth muscle physiology, Adenine, Calcium channels, Vascular smooth muscle contraction |
| Abstract: | Aim Rats with adenine-induced chronic renal failure (A- CRF) develop a reduced rate of relaxation of the thoracic aorta. The aim of this study was to elucidate the mechanisms underlying this abnormality. Methods Male Sprague Dawley rats received either chow containing adenine or were pair-fed with normal chow (controls). After 8-14 weeks, arterial function was analysed ex vivo using wire myography and the expression of proteins involved in vascular smooth muscle excitation-contraction coupling in the thoracic aorta was analysed. Results The rate of relaxation following washout of KCl was reduced in A- CRF rats vs. controls in the thoracic aorta ( P < 0.01), abdominal aorta ( P < 0.05), and common carotid artery ( P < 0.05), but not in the common femoral artery. Relaxation rates of thoracic aortas increased ( P < 0.01), but were not normalized, in response to washout of KCl with Ca2+-free buffer. Microarray and qRT- PCR analyses of genes involved in excitation-contraction coupling identified 10 genes, which showed significantly altered expression in A- CRF thoracic aortas. At the protein level, the α2 subunit of the Na,K- ATPase ( P < 0.001) and SERCA2 ( P < 0.05) was significantly downregulated, whereas stromal interaction molecule 1 and calsequestrin-1 and calsequestrin-2 were significantly upregulated ( P < 0.05). Conclusions Rats with A- CRF show a marked alteration in relaxation of larger conduit arteries localized proximal to the common femoral artery. This abnormality may be caused by reduced cytosolic Ca2+ clearance in vascular smooth muscle cells secondary to dysregulation of proteins crucially involved in this process. [ABSTRACT FROM AUTHOR] |
| Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.) | |
| Database: | Psychology and Behavioral Sciences Collection |
| FullText | Links: – Type: pdflink Text: Availability: 0 |
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| Header | DbId: pbh DbLabel: Psychology and Behavioral Sciences Collection An: 119354320 AccessLevel: 6 PubType: Academic Journal PubTypeId: academicJournal PreciseRelevancyScore: 0 |
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| Items | – Name: Title Label: Title Group: Ti Data: Adenine-induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling. – Name: Author Label: Authors Group: Au Data: <searchLink fieldCode="AR" term="%22Nguy%2C+L%2E%22">Nguy, L.</searchLink><br /><searchLink fieldCode="AR" term="%22Shubbar%2C+E%2E%22">Shubbar, E.</searchLink><br /><searchLink fieldCode="AR" term="%22Jernås%2C+M%2E%22">Jernås, M.</searchLink><br /><searchLink fieldCode="AR" term="%22Nookaew%2C+I%2E%22">Nookaew, I.</searchLink><br /><searchLink fieldCode="AR" term="%22Lundgren%2C+J%2E%22">Lundgren, J.</searchLink><br /><searchLink fieldCode="AR" term="%22Olsson%2C+B%2E%22">Olsson, B.</searchLink><br /><searchLink fieldCode="AR" term="%22Nilsson%2C+H%2E%22">Nilsson, H.</searchLink><br /><searchLink fieldCode="AR" term="%22Guron%2C+G%2E%22">Guron, G.</searchLink> – Name: TitleSource Label: Source Group: Src Data: <searchLink fieldCode="JN" term="%22Acta+Physiologica%22">Acta Physiologica</searchLink>. Dec2016, Vol. 218 Issue 4, p250-264. 15p. – Name: Subject Label: Subjects Group: Su Data: <searchLink fieldCode="DE" term="%22Treatment+of+chronic+kidney+failure%22">Treatment of chronic kidney failure</searchLink><br /><searchLink fieldCode="DE" term="%22Protein+expression%22">Protein expression</searchLink><br /><searchLink fieldCode="DE" term="%22Vascular+smooth+muscle+physiology%22">Vascular smooth muscle physiology</searchLink><br /><searchLink fieldCode="DE" term="%22Adenine%22">Adenine</searchLink><br /><searchLink fieldCode="DE" term="%22Calcium+channels%22">Calcium channels</searchLink><br /><searchLink fieldCode="DE" term="%22Vascular+smooth+muscle+contraction%22">Vascular smooth muscle contraction</searchLink> – Name: Abstract Label: Abstract Group: Ab Data: Aim Rats with adenine-induced chronic renal failure (A- CRF) develop a reduced rate of relaxation of the thoracic aorta. The aim of this study was to elucidate the mechanisms underlying this abnormality. Methods Male Sprague Dawley rats received either chow containing adenine or were pair-fed with normal chow (controls). After 8-14 weeks, arterial function was analysed ex vivo using wire myography and the expression of proteins involved in vascular smooth muscle excitation-contraction coupling in the thoracic aorta was analysed. Results The rate of relaxation following washout of KCl was reduced in A- CRF rats vs. controls in the thoracic aorta ( P < 0.01), abdominal aorta ( P < 0.05), and common carotid artery ( P < 0.05), but not in the common femoral artery. Relaxation rates of thoracic aortas increased ( P < 0.01), but were not normalized, in response to washout of KCl with Ca2+-free buffer. Microarray and qRT- PCR analyses of genes involved in excitation-contraction coupling identified 10 genes, which showed significantly altered expression in A- CRF thoracic aortas. At the protein level, the α2 subunit of the Na,K- ATPase ( P < 0.001) and SERCA2 ( P < 0.05) was significantly downregulated, whereas stromal interaction molecule 1 and calsequestrin-1 and calsequestrin-2 were significantly upregulated ( P < 0.05). Conclusions Rats with A- CRF show a marked alteration in relaxation of larger conduit arteries localized proximal to the common femoral artery. This abnormality may be caused by reduced cytosolic Ca2+ clearance in vascular smooth muscle cells secondary to dysregulation of proteins crucially involved in this process. [ABSTRACT FROM AUTHOR] – Name: AbstractSuppliedCopyright Label: Group: Ab Data: <i>Copyright of Acta Physiologica is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.) |
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| RecordInfo | BibRecord: BibEntity: Identifiers: – Type: doi Value: 10.1111/apha.12724 Languages: – Code: eng Text: English PhysicalDescription: Pagination: PageCount: 15 StartPage: 250 Subjects: – SubjectFull: Treatment of chronic kidney failure Type: general – SubjectFull: Protein expression Type: general – SubjectFull: Vascular smooth muscle physiology Type: general – SubjectFull: Adenine Type: general – SubjectFull: Calcium channels Type: general – SubjectFull: Vascular smooth muscle contraction Type: general Titles: – TitleFull: Adenine-induced chronic renal failure in rats decreases aortic relaxation rate and alters expression of proteins involved in vascular smooth muscle calcium handling. Type: main BibRelationships: HasContributorRelationships: – PersonEntity: Name: NameFull: Nguy, L. – PersonEntity: Name: NameFull: Shubbar, E. – PersonEntity: Name: NameFull: Jernås, M. – PersonEntity: Name: NameFull: Nookaew, I. – PersonEntity: Name: NameFull: Lundgren, J. – PersonEntity: Name: NameFull: Olsson, B. – PersonEntity: Name: NameFull: Nilsson, H. – PersonEntity: Name: NameFull: Guron, G. IsPartOfRelationships: – BibEntity: Dates: – D: 01 M: 12 Text: Dec2016 Type: published Y: 2016 Identifiers: – Type: issn-print Value: 17481708 Numbering: – Type: volume Value: 218 – Type: issue Value: 4 Titles: – TitleFull: Acta Physiologica Type: main |
| ResultId | 1 |
