Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Renal sympathetic denervation improves cardiac dysfunction in rats with chronic pressure overload

Z. Z. Li, H. Jiang, D. Chen, Q. Liu, J. Geng, J. Q. Guo, R. H. Sun, G. Q. Zhu, Q. J. Shan

. 2015 ; 64 (5) : 653-662. [pub] 2015Mar24

Language English Country Czech Republic

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc16031098

Varied causative and risk factors can lead to cardiac dysfunction. Cardiac dysfunction often evolves into heart failure by cardiac remodeling due to autonomic nervous system disturbance and neurohumoral abnormalities, even if the detriment factors are removed. Renal sympathetic nerve activity plays a pivotal regulatory role in neurohumoral mechanisms. The present study was designed to determine the therapeutic effects of renal sympathetic denervation (RSD) on cardiac dysfunction, fibrosis, and neurohumoral response in transverse aortic constriction (TAC) rats with chronic pressure overload. The present study demonstrated that RSD attenuated myocardial fibrosis and hypertrophy, and structural remodeling of the left atrium and ventricle, up-regulated cardiac beta adrenoceptor (beta-AR, including beta(1)AR and beta(2)AR) and sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) while down-regulated angiotensin II type 1 receptor (AT(1)R), and decreased plasma B-type natriuretic peptide (BNP), norepinephrine (NE), angiotensin II (Ang II), and arginine vasopressin (AVP) levels in TAC rats with chronic pressure overload. We conclude that RSD attenuates myocardial fibrosis, the left atrial enlargement, and the left ventricular wall hypertrophy; inhibits the overdrive of the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and AVP system in TAC rats with chronic pressure overload. RSD could be a promising non-pharmacological approach to control the progression of cardiac dysfunction.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc16031098
003      
CZ-PrNML
005      
20161111143315.0
007      
ta
008      
161101s2015 xr ad f 000 0|ENG||
009      
AR
024    7_
$a 10.33549/physiolres.932912 $2 doi
035    __
$a (PubMed)25804096
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a ENG
044    __
$a xr
100    1_
$a Li, Z.-Z. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
245    10
$a Renal sympathetic denervation improves cardiac dysfunction in rats with chronic pressure overload / $c Z. Z. Li, H. Jiang, D. Chen, Q. Liu, J. Geng, J. Q. Guo, R. H. Sun, G. Q. Zhu, Q. J. Shan
520    9_
$a Varied causative and risk factors can lead to cardiac dysfunction. Cardiac dysfunction often evolves into heart failure by cardiac remodeling due to autonomic nervous system disturbance and neurohumoral abnormalities, even if the detriment factors are removed. Renal sympathetic nerve activity plays a pivotal regulatory role in neurohumoral mechanisms. The present study was designed to determine the therapeutic effects of renal sympathetic denervation (RSD) on cardiac dysfunction, fibrosis, and neurohumoral response in transverse aortic constriction (TAC) rats with chronic pressure overload. The present study demonstrated that RSD attenuated myocardial fibrosis and hypertrophy, and structural remodeling of the left atrium and ventricle, up-regulated cardiac beta adrenoceptor (beta-AR, including beta(1)AR and beta(2)AR) and sarco-endoplasmic reticulum Ca(2+)-ATPase (SERCA) while down-regulated angiotensin II type 1 receptor (AT(1)R), and decreased plasma B-type natriuretic peptide (BNP), norepinephrine (NE), angiotensin II (Ang II), and arginine vasopressin (AVP) levels in TAC rats with chronic pressure overload. We conclude that RSD attenuates myocardial fibrosis, the left atrial enlargement, and the left ventricular wall hypertrophy; inhibits the overdrive of the sympathetic nervous system (SNS), renin-angiotensin-aldosterone system (RAAS), and AVP system in TAC rats with chronic pressure overload. RSD could be a promising non-pharmacological approach to control the progression of cardiac dysfunction.
650    _2
$a zvířata $7 D000818
650    _2
$a chronická nemoc $7 D002908
650    _2
$a srdeční selhání $x metabolismus $x patofyziologie $x chirurgie $7 D006333
650    _2
$a hypertrofie levé komory srdeční $x metabolismus $x patofyziologie $x chirurgie $7 D017379
650    _2
$a ledviny $x inervace $x chirurgie $7 D007668
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a kardiomyocyty $x patologie $x fyziologie $7 D032383
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani Sprague-Dawley $7 D017207
650    _2
$a renin-angiotensin systém $x fyziologie $7 D012084
650    _2
$a sympatektomie $x trendy $7 D013562
650    _2
$a sympatický nervový systém $x patologie $x fyziologie $7 D013564
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Jiang, H. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
700    1_
$a Chen, D. $u Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu, China
700    1_
$a Liu, Q. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
700    1_
$a Geng, J. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
700    1_
$a Guo, J.-Q. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
700    1_
$a Sun, R.-H. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
700    1_
$a Zhu, G.-Q. $u Key Laboratory of Cardiovascular Disease and Molecular Intervention, Department of Physiology, Nanjing Medical University, Nanjing, Jiangsu, China
700    1_
$a Shan, Q.-J. $u Cardiovascular Department, First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu, China,
773    0_
$w MED00003824 $t Physiological research $x 1802-9973 $g Roč. 64, č. 5 (2015), s. 653-662
856    41
$u http://www.biomed.cas.cz/physiolres/ $y domovská stránka časopisu
910    __
$a ABA008 $b A 4120 $c 266 $y 4 $z 0
990    __
$a 20161101 $b ABA008
991    __
$a 20161110094430 $b ABA008
999    __
$a ok $b bmc $g 1172186 $s 955756
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2015 $b 64 $c 5 $d 653-662 $e 2015Mar24 $i 1802-9973 $m Physiological research $n Physiol. Res. (Print) $x MED00003824
LZP    __
$b NLK118 $a Pubmed-20161101
Back

Find record

Citation metrics

Archiving options