ArticleCanadian journal of physiology and pharmacology2011
Regulation of L-type inward calcium channel activity by captopril and angiotensin II via the phosphatidyl inositol 3-kinase pathway in cardiomyocytes from volume-overload hypertrophied rat hearts.
Article in Canadian journal of physiology and pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Impact of the Renin-Angiotensin System on the Pathogeny and Pharmacotherapeutics of Neurodegenerative Diseases.Biomolecules · 2022Review
- Interactions Among Brain-Derived Neurotrophic Factor and Neuroimmune Pathways Are Key Components of the Major Psychiatric Disorders.Molecular neurobiology · 2022Review
- Hypertension: Potential Player in Cardiovascular Disease Incidence in Preeclampsia.Cardiovascular toxicology · 2022Review
- Atrial Electrical Remodeling in Mice With Cardiac-Specific Overexpression of Angiotensin II Type 1 Receptor.Journal of the American Heart Association · 2022Article
- Effects of Trandolapril on Structural, Contractile and Electrophysiological Remodeling in Experimental Volume Overload Heart Failure.Frontiers in pharmacology · 2021Article
- Inhibition of Autophagy by Captopril Attenuates Prion Peptide-Mediated Neuronal Apoptosis via AMPK Activation.Molecular neurobiology · 2019Article
- Critical role of angiotensin II type 2 receptors in the control of mitochondrial and cardiac function in angiotensin II-preconditioned rat hearts.Pflugers Archiv : European journal of physiology · 2018Article
- Brain-derived neurotrophic factor reduces inflammation and hippocampal apoptosis in experimental Streptococcus pneumoniae meningitis.Journal of neuroinflammation · 2017Article
- Anaphylatoxins Activate CaFrontiers in immunology · 2017Article
- Angiotensin II-Induced Apoptosis of Human Umbilical Vein Endothelial Cells was Inhibited by Blueberry Anthocyanin Through Bax- and Caspase 3-Dependent Pathways.Medical science monitor : international medical journal of experimental and clinical research · 2016Article
- Rapid multislice T1 mapping of mouse myocardium: Application to quantification of manganese uptake in α-Dystrobrevin knockout mice.Magnetic resonance in medicine · 2015Article
- Rutaecarpine inhibits angiotensin II-induced proliferation in rat vascular smooth muscle cells.Chinese journal of integrative medicine · 2014Article
- The effect of captopril and losartan on the electrophysiology of myocardial cells of myocardial ischemia rats.International journal of clinical and experimental medicine · 2014Article
- Calcitonin Gene-Related Peptide Regulates Cardiomyocyte Survival through Regulation of Oxidative Stress by PI3K/Akt and MAPK Signaling Pathways.Annals of clinical and experimental hypertension · 2014Article
- MRI biomarkers for evaluation of treatment efficacy in preclinical diabetic retinopathy.Expert opinion on medical diagnostics · 2013Review
- Inotropic and lusitropic effects of calcitonin gene-related peptide in the heart.American journal of physiology. Heart and circulatory physiology · 2013Article
- Endothelin-1 stimulates the expression of L-type Ca2+ channels in neonatal rat cardiomyocytes via the extracellular signal-regulated kinase 1/2 pathway.The Journal of membrane biology · 2013Article
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
Abstract
Heart failure can be caused by pro-hypertrophic humoral factors such as angiotensin II (Ang II), which regulates protein kinase activities. The intermingled responses of these kinases lead to the early compensated cardiac hypertrophy, but later to the uncompensated phase of heart failure. We have shown that although beneficial, cardiac hypertrophy is associated with modifications in ion channels that are mainly mediated through mitogen-activated protein (MAP) kinase and phosphatidylinositol 3-kinase (PI3K) activation. This study evaluates the control of L-type Ca(2+) current (I(Ca,L)) by the Ang II/PI3K pathway in hypertrophied ventricular myocytes from volume-overload rats using the perforated patch-clamp technique. To assess activation of the I(Ca,L) in cardiomyocytes, voltages of 350 ms in 10 mV increments from a holding potential of -85 mV were applied to cardiocytes, with a pre-pulse to -45 mV for 300 ms. Volume overload-induced hypertrophy reduces I(Ca,L), whereas addition of Ang II alleviates the hypertrophic-induced decrease in a PI3K-dependent manner. Acute administration of Ang II (10(-6) mol/L) to normal adult cardiomyocytes had no effect; however, captopril reduced their basal I(Ca,L). In parallel, captopril regressed the hypertrophy and inverted the Ang II effect on I(Ca,L) seemingly through a PI3K upstream effector. Thus, it seems that regression of cardiac hypertrophy by captopril improved I(Ca,L) partly through PI3K.
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