ArticleHypertension (Dallas, Tex. : 1979)2010
Role of phosphoinositide 3-kinase {alpha}, protein kinase C, and L-type Ca2+ channels in mediating the complex actions of angiotensin II on mouse cardiac contractility.
Article in Hypertension (Dallas, Tex. : 1979), 2010. 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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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 27 citations in OpenAlex.
- Understanding the distinct role of PI3K(p110Frontiers in cardiovascular medicine · 2026Review
- PI3K(p110α) as a determinant and gene therapy for atrial enlargement in atrial fibrillation.Molecular and cellular biochemistry · 2023Review
- Bidirectional regulatory effects of Cordyceps on arrhythmia: Clinical evaluations and network pharmacology.Frontiers in pharmacology · 2022Article
- Role of PI3K/Akt signaling pathway in cardiac fibrosis.Molecular and cellular biochemistry · 2021Review
- Cardiomyocyte-specific deletion of β-catenin protects mouse hearts from ventricular arrhythmias after myocardial infarction.Scientific reports · 2021Article
- Association of Regulatory Genetic Variants for Protein Kinase Cα with Mortality and Drug Efficacy in Patients with Heart Failure.Cardiovascular drugs and therapy · 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
- The effect of angiotensin II on blood pressure in patients with circulatory shock: a structured review of the literature.Critical care (London, England) · 2017Review
- Angiotensin II activates CaThe Journal of physiology · 2017Article
- Phosphoinositide 3-kinase: friend and foe in cardiovascular disease.Frontiers in pharmacology · 2015Review
- Importance of cell-cell contact in the therapeutic benefits of cardiosphere-derived cells.Stem cells (Dayton, Ohio) · 2014Article
- Mural propagation of descending vasa recta responses to mechanical stimulation.American journal of physiology. Renal physiology · 2013Article
- Hydrogen peroxide differentially modulates cardiac myocyte nitric oxide synthesis.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Different roles of membrane potentials in electrotaxis and chemotaxis of dictyostelium cells.Eukaryotic cell · 2011Article
- Specific PI3K isoform modulation in heart failure: lessons from transgenic mice.Current heart failure reports · 2011Review
- G protein-dependent and G protein-independent signaling pathways and their impact on cardiac function.Circulation research · 2011Review
- The long and short of PKC modulation of the L-type calcium channel.Channels (Austin, Tex.)Article
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8 authors at 6 institutions in 2 countries.
Funding
Abstract
Although angiotensin II (Ang II) plays an important role in heart disease associated with pump dysfunction, its direct effects on cardiac pump function remain controversial. We found that after Ang II infusion, the developed pressure and +dP/dt(max) in isolated Langendorff-perfused mouse hearts showed a complex temporal response, with a rapid transient decrease followed by an increase above baseline. Similar time-dependent changes in cell shortening and L-type Ca(2+) currents were observed in isolated ventricular myocytes. Previous studies have established that Ang II signaling involves phosphoinositide 3-kinases (PI3K). Dominant-negative inhibition of PI3Kalpha in the myocardium selectively eliminated the rapid negative inotropic action of Ang II (inhibited by approximately 90%), whereas the loss of PI3Kgamma had no effect on the response to Ang II. Consistent with a link between PI3Kalpha and protein kinase C (PKC), PKC inhibition (with GF 109203X) reduced the negative inotropic effects of Ang II by approximately 50%. Although PI3Kalpha and PKC activities are associated with glycogen synthase kinase-3beta and NADPH oxidase, genetic ablation of either glycogen synthase kinase-3beta or p47(phox) (an essential subunit of NOX2-NADPH oxidase) had no effect on the inotropic actions of Ang II. Our results establish that Ang II has complex temporal effects on contractility and L-type Ca(2+) channels in normal mouse myocardium, with the negative inotropic effects requiring PI3Kalpha and PKC activities.
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