Literature DB >> 28078053

Amyloid beta peptide 22-35 induces a negative inotropic effect on isolated rat hearts.

Neda Yousefirad1, Ziya Kaygısız1, Yasemin Aydın1.   

Abstract

Evidences indicate that deposition of amyloid beta peptides (Aβs) plays an important role in the pathogenesis of Alzheimer disease. Aβs may influence cardiovascular system and ileum contractions. But the effect of amyloid beta peptide 22-35 (Aβ22-35) on cardiovascular functions and contractions of ileum has not been studied. Therefore, the present study aimed to investigate the possible effects of this peptide on isolated rat heart and ileum smooth muscle. Langendorff-perfused rat heart preparations were established. The hearts were perfused under constant pressure (60 mmHg) with modified Krebs-Henseleit solution. Aβ22-35 at doses of 1, 10 and 100 nM significantly decreased left ventricular developed pressure (LVDP; an index of cardiac contractility) and maximal rate of pressure development of left ventricle (+dP/dtmax; another index of cardiac contractility). This peptide at doses studied had no significant effect on heart rate, coronary flow, monophasic action potential amplitude (MAPamp), MAP duration at 90% repolarization (MAP90) and ileum contractions. We suggest that Aβ22-35 exerts a negative inotropism on isolated rat hearts with unchanged heart rate, coronary flow, MAPamp, MAP90 and smooth muscle contractility of ileum.

Entities:  

Keywords:  Amyloid beta peptide 22-35; cardiac contractility; coronary flow; heart rate; ileum contraction; monophasic action potential

Year:  2016        PMID: 28078053      PMCID: PMC5209443     

Source DB:  PubMed          Journal:  Int J Physiol Pathophysiol Pharmacol        ISSN: 1944-8171


  27 in total

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Authors:  M Di Carlo; D Giacomazza; P L San Biagio
Journal:  J Phys Condens Matter       Date:  2012-05-18       Impact factor: 2.333

Review 4.  Cerebral hypoperfusion and glucose hypometabolism: Key pathophysiological modulators promote neurodegeneration, cognitive impairment, and Alzheimer's disease.

Authors:  Mak Adam Daulatzai
Journal:  J Neurosci Res       Date:  2016-06-27       Impact factor: 4.164

5.  Dauricine-induced changes in monophasic action potentials and effective refractory period of rabbit left ventricle in situ.

Authors:  Jing-Sheng Xia; Zhen Li; Jian-Wen Dong; Hong Tu; Fan-Dian Zeng
Journal:  Acta Pharmacol Sin       Date:  2002-04       Impact factor: 6.150

Review 6.  The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics.

Authors:  John Hardy; Dennis J Selkoe
Journal:  Science       Date:  2002-07-19       Impact factor: 47.728

7.  Amyloid-β protein impairs Ca2+ release and contractility in skeletal muscle.

Authors:  Alexander Shtifman; Christopher W Ward; Derek R Laver; Mark L Bannister; Jose R Lopez; Masashi Kitazawa; Frank M LaFerla; Noriaki Ikemoto; Henry W Querfurth
Journal:  Neurobiol Aging       Date:  2008-12-23       Impact factor: 4.673

Review 8.  Motor impairment in Alzheimer's disease and transgenic Alzheimer's disease mouse models.

Authors:  O Wirths; T A Bayer
Journal:  Genes Brain Behav       Date:  2008-02       Impact factor: 3.449

9.  Alzheimer's beta-amyloid-induced depolarization of skeletal muscle fibers: implications for motor dysfunctions in dementia.

Authors:  Marat A Mukhamedyarov; Sergey N Grishin; Elvina R Yusupova; Andrey L Zefirov; András Palotás
Journal:  Cell Physiol Biochem       Date:  2009-02-18

10.  Cardiomyocyte contractile dysfunction in the APPswe/PS1dE9 mouse model of Alzheimer's disease.

Authors:  Subat Turdi; Rui Guo; Anna F Huff; Eliza M Wolf; Bruce Culver; Jun Ren
Journal:  PLoS One       Date:  2009-06-24       Impact factor: 3.240

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