-
Je něco špatně v tomto záznamu ?
Antioxidant/oxidant status and cardiac function in bradykinin B(1)- and B(2)-receptor null mice
S. Delemasure, N. Blaes, C. Richard, R. Couture, M. Bader, P. Dutartre, JP. Girolami, JL. Connat, L. Rochette
Jazyk angličtina Země Česko
Typ dokumentu časopisecké články, práce podpořená grantem
NLK
Directory of Open Access Journals
od 1991
Free Medical Journals
od 1998
ProQuest Central
od 2005-01-01
Medline Complete (EBSCOhost)
od 2006-01-01
Nursing & Allied Health Database (ProQuest)
od 2005-01-01
Health & Medicine (ProQuest)
od 2005-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1998
- MeSH
- antioxidancia metabolismus MeSH
- biologické markery krev MeSH
- dysfunkce levé srdeční komory krev genetika metabolismus patofyziologie MeSH
- funkce levé komory srdeční * MeSH
- kontrakce myokardu * MeSH
- kyselina dehydroaskorbová analogy a deriváty krev MeSH
- myokard metabolismus MeSH
- myši inbrední C57BL MeSH
- myši kmene 129 MeSH
- myši knockoutované MeSH
- myši MeSH
- oxidační stres * MeSH
- pulzní dopplerovská echokardiografie MeSH
- receptor bradykininu B1 nedostatek genetika MeSH
- receptor bradykininu B2 nedostatek genetika MeSH
- zvířata MeSH
- Check Tag
- mužské pohlaví MeSH
- myši MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
Kinin-vasoactive peptides activate two G-protein-coupled receptors (R), B(1)R (inducible) and B(2)R (constitutive). Their complex role in cardiovascular diseases could be related to differential actions on oxidative stress. This study investigated impacts of B(1)R or B(2)R gene deletion in mice on the cardiac function and plasma antioxidant and oxidant status. Echocardiography-Doppler was performed in B(1)R (B(1)R(-/-)) and B(2)R (B(2)R(-/-)) deficient and wild type (WT) adult male mice. No functional alteration was observed in B(2)R(-/-) hearts. B(1)R(-/-) mice had significantly lowered fractional shortening and increased isovolumetric contraction time. The diastolic E and A waves velocity ratio was similar in all mice groups. Thus B(1)R(-/-) mice provide a model of moderate systolic dysfunction, whereas B(2)R(-/-) mice displayed a normal cardiac phenotype. Plasma antioxidant capacity (ORAC) was significantly decreased in both B(1)R(-/-) and B(2)R(-/-) mice whereas the vitamin C levels were decreased in B(2)R(-/-) mice only. Plasma ascorbyl free radical was significantly higher in B(1)R(-/-) compared to WT and B(2)R(-/-) mice. Therefore, the oxidative stress index, ascorbyl free radical to vitamin C ratio, was increased in both B(1)R(-/-) and B(2)R(-/-) mice. Hence, B(1)R and B(2)R deficiency are associated with increased oxidative stress, but there is a differential imbalance between free radical production and antioxidant defense. The interrelationship between the differential B(1)R and B(2)R roles in oxidative stress and cardiovascular diseases remain to be investigated.
COHIRO Biotechnology Faculty of Medicine Dijon France
Department of Physiology Faculty of Medicine Université de Montréal Montréal Qc Canada
Citace poskytuje Crossref.org
- 000
- 00000naa a2200000 a 4500
- 001
- bmc14066029
- 003
- CZ-PrNML
- 005
- 20140731110226.0
- 007
- ta
- 008
- 140722s2013 xr d f 000 0|eng||
- 009
- AR
- 024 7_
- $a 10.33549/physiolres.932496 $2 doi
- 035 __
- $a (PubMed)24020815
- 040 __
- $a ABA008 $b cze $d ABA008 $e AACR2
- 041 0_
- $a eng
- 044 __
- $a xr
- 100 1_
- $a Delemasure, S. $u COHIRO Biotechnology, Faculty of Medicine, Dijon, France
- 245 10
- $a Antioxidant/oxidant status and cardiac function in bradykinin B(1)- and B(2)-receptor null mice / $c S. Delemasure, N. Blaes, C. Richard, R. Couture, M. Bader, P. Dutartre, JP. Girolami, JL. Connat, L. Rochette
- 520 9_
- $a Kinin-vasoactive peptides activate two G-protein-coupled receptors (R), B(1)R (inducible) and B(2)R (constitutive). Their complex role in cardiovascular diseases could be related to differential actions on oxidative stress. This study investigated impacts of B(1)R or B(2)R gene deletion in mice on the cardiac function and plasma antioxidant and oxidant status. Echocardiography-Doppler was performed in B(1)R (B(1)R(-/-)) and B(2)R (B(2)R(-/-)) deficient and wild type (WT) adult male mice. No functional alteration was observed in B(2)R(-/-) hearts. B(1)R(-/-) mice had significantly lowered fractional shortening and increased isovolumetric contraction time. The diastolic E and A waves velocity ratio was similar in all mice groups. Thus B(1)R(-/-) mice provide a model of moderate systolic dysfunction, whereas B(2)R(-/-) mice displayed a normal cardiac phenotype. Plasma antioxidant capacity (ORAC) was significantly decreased in both B(1)R(-/-) and B(2)R(-/-) mice whereas the vitamin C levels were decreased in B(2)R(-/-) mice only. Plasma ascorbyl free radical was significantly higher in B(1)R(-/-) compared to WT and B(2)R(-/-) mice. Therefore, the oxidative stress index, ascorbyl free radical to vitamin C ratio, was increased in both B(1)R(-/-) and B(2)R(-/-) mice. Hence, B(1)R and B(2)R deficiency are associated with increased oxidative stress, but there is a differential imbalance between free radical production and antioxidant defense. The interrelationship between the differential B(1)R and B(2)R roles in oxidative stress and cardiovascular diseases remain to be investigated.
- 650 _2
- $a zvířata $7 D000818
- 650 _2
- $a antioxidancia $x metabolismus $7 D000975
- 650 _2
- $a biologické markery $x krev $7 D015415
- 650 _2
- $a kyselina dehydroaskorbová $x analogy a deriváty $x krev $7 D003683
- 650 _2
- $a pulzní dopplerovská echokardiografie $7 D018619
- 650 _2
- $a mužské pohlaví $7 D008297
- 650 _2
- $a myši $7 D051379
- 650 _2
- $a myši kmene 129 $7 D057507
- 650 _2
- $a myši inbrední C57BL $7 D008810
- 650 _2
- $a myši knockoutované $7 D018345
- 650 12
- $a kontrakce myokardu $7 D009200
- 650 _2
- $a myokard $x metabolismus $7 D009206
- 650 12
- $a oxidační stres $7 D018384
- 650 _2
- $a receptor bradykininu B1 $x nedostatek $x genetika $7 D043783
- 650 _2
- $a receptor bradykininu B2 $x nedostatek $x genetika $7 D043782
- 650 _2
- $a dysfunkce levé srdeční komory $x krev $x genetika $x metabolismus $x patofyziologie $7 D018487
- 650 12
- $a funkce levé komory srdeční $7 D016277
- 655 _2
- $a časopisecké články $7 D016428
- 655 _2
- $a práce podpořená grantem $7 D013485
- 700 1_
- $a Blaes, N. $u Institute of Metabolic and Cardiovascular Diseases (I2MC), INSERM, U1048, Université Paul Sabatier, Toulouse, France
- 700 1_
- $a Richard, C. $u Laboratory of Cardio-Metabolic Pathophysiology and Pharmacology (LPPCM), INSERM, U866, Université de Bourgogne, Dijon, France; Laboratory of Cardio-Metabolic Pathophysiology and Pharmacology (LPPCM), INSERM, U866, Université de Bourgogne, Dijon, France
- 700 1_
- $a Couture, R. $u Department of Physiology, Faculty of Medicine, Université de Montréal, Montréal, Qc, Canada
- 700 1_
- $a Bader, M. $u Max-Delbrück-Center for Molecular Medicine, Berlin, Germany
- 700 1_
- $a Dutartre, P. $u COHIRO Biotechnology, Faculty of Medicine, Dijon, France; Laboratory of Cardio-Metabolic Pathophysiology and Pharmacology (LPPCM), INSERM, U866, Université de Bourgogne, Dijon, France
- 700 1_
- $a Girolami, J.-P. $u Institute of Metabolic and Cardiovascular Diseases (I2MC), INSERM, U1048, Université Paul Sabatier, Toulouse, France
- 700 1_
- $a Connat, J.-L. $u COHIRO Biotechnology, Faculty of Medicine, Dijon, France; Laboratory of Cardio-Metabolic Pathophysiology and Pharmacology (LPPCM), INSERM, U866, Université de Bourgogne, Dijon, France
- 700 1_
- $a Rochette, L. $u COHIRO Biotechnology, Faculty of Medicine, Dijon, France; Laboratory of Cardio-Metabolic Pathophysiology and Pharmacology (LPPCM), INSERM, U866, Université de Bourgogne, Dijon, France
- 773 0_
- $w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 62, č. 5 (2013), s. 511-517
- 856 41
- $u http://www.biomed.cas.cz/physiolres/archive.htm $y domovská stránka časopisu - plný text volně přístupný
- 910 __
- $a ABA008 $b A 4120 $c 266 $y 4 $z 0
- 990 __
- $a 20140722 $b ABA008
- 991 __
- $a 20140730074817 $b ABA008
- 999 __
- $a ok $b bmc $g 1034313 $s 864805
- BAS __
- $a 3
- BAS __
- $a PreBMC
- BMC __
- $a 2013 $b 62 $c 5 $d 511-517 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
- LZP __
- $b NLK118 $a Pubmed-20140722