ArticleMolecular and cellular biochemistry2007
Impaired cell communication in the diabetic heart. The role of the renin angiotensin system.
Article in Molecular and cellular biochemistry, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 18 citations in OpenAlex.
- Sulforaphane inhibits angiotensin II-induced cardiomyocyte apoptosis by acetylation modification of Nrf2.Aging · 2022Article
- Advanced Glycation End Product (AGE)-AGE Receptor (RAGE) System Upregulated Connexin43 Expression in Rat Cardiomyocytes via PKC and Erk MAPK Pathways.International journal of molecular sciences · 2013Article
- Cardiovascular disease risk in the offspring of diabetic women: the impact of the intrauterine environment.Experimental diabetes research · 2012Review
- Oxidative-dependent integration of signal transduction with intercellular gap junctional communication in the control of gene expression.Antioxidants & redox signaling · 2009Review
- Gap junction channels exhibit connexin-specific permeability to cyclic nucleotides.The Journal of general physiology · 2008Article
- Propagation of the cardiac impulse in the diabetic rat heart: reduced conduction reserve.The Journal of physiology · 2007Article
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Abstract
The influence of diabetes mellitus on the process of cell communication and impulse propagation was investigated in trabeculae isolated from the ventricle of diabetic rat hearts. Diabetes was produced by a single intraperitoneal injection of streptozotocin (60 mg/Kg). Cell-to-cell spread of Lucifer yellow CH was studied with the cut-end method. Measurements of the diffusion coefficient of Lucifer Yellow CH (D) was made by fitting the experimental results to theoretical points using an interactive computer program for non-linear regression. The results indicated an average value of D of 3 +/- 0.8x10(-7 )cm(2)/s for the controls (n = 5) and 3.8 +/- 0.5x10(-8 )cm(2)/s (n = 7) (p < 0.05) for diabetic hearts. No change of efflux of the dye through the surface cell membrane was found in diabetic rat compared to controls (p > 0.05). Moreover, the dye binding in the cytosol of diabetic heart was not significantly different from controls. The calculated values of junctional permeability for the dye was found to be p (j) = 1.5x10(-3 )cm/s for control and 1.5x10(-5 )cm/s for diabetic heart. To investigate the possible role of the activation of the renin-angiotensin system (RAS) on the change in cell communication, diabetic rats were treated with enalapril (25 mg/Kg/day) for a period of 14 days. Measurements of the diffusion coefficient (D) of the dye indicated a significant increase of D (6.7 +/- 1.1x10(-7 )cm(2)/s) (n = 4) (p < 0.05) compared with diabetic rats not exposed to enalapril. No change on efflux of the dye or cytoplasmic binding was found in animals treated with enalapril. The calculated value of junctional permeability showed a significant increase (p (j) = 3.9x10(-4 )cm/s) in presence of enalapril compared with controls. In addition, angiotensin II (10(-8 )M) added to the bath caused a significant decrease of conduction velocity in cardiac muscle of diabetic heart. In conclusion, Cell communication and impulse propagation are significantly impaired in the ventricle from diabetic rats, a phenomenon partly related to the activation of the RAS.
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