The Anrep effect: 100 years later

Cingolani, Horacio E.; Pérez, Néstor Gustavo; Cingolani, Oscar H.; Ennis, Irene L.

doi:10.1152/ajpheart.00508.2012

Cited by 137 publications

(123 citation statements)

References 81 publications

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“…Similar results were obtained when this technique was used to silence the NHE1 by direct injection of a naked interference RNA in the left ventricular wall. 10 Because we have previously shown that the SFR to myocardial stretch is the mechanical counterpart of an autocrine/ paracrine mechanism triggered by the release of endogenous angiotensin II (Ang II) involving MR and NHE1 activation, 11 we decided to functionally test the MR under our experimental conditions by exploring the SFR and NHE1 activation after stretching isolated papillary muscles from l-shMR-and control-injected hearts. The stretching of the papillary muscles in the control group promoted the characteristic biphasic mechanical response, an initial abrupt force increase followed by the SFR (Figure 3A-3C).…”

Section: Resultsmentioning

confidence: 99%

Myocardial Mineralocorticoid Receptor Activation by Stretching and Its Functional Consequences

et al. 2014

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Abstract-Myocardial stretch triggers an angiotensin II-dependent autocrine/paracrine loop of intracellular signals, leading to reactive oxygen species-mediated activation of redox-sensitive kinases. Based on pharmacological strategies, we previously proposed that mineralocorticoid receptor (MR) is necessary for this stretch-triggered mechanism. Now, we aimed to test the role of MR after stretch by using a molecular approach to avoid secondary effects of pharmacological MR blockers. Small hairpin interference RNA capable of specifically knocking down the MR was incorporated into a lentiviral vector (l-shMR) and injected into the left ventricular wall of Wistar rats. The same vector but expressing a nonsilencing sequence (scramble) was used as control. Lentivirus propagation through the left ventricle was evidenced by confocal microscopy. Myocardial MR expression, stretch-triggered activation of redoxsensitive kinases (ERK1/2-p90 RSK ), the consequent Na + /H + exchanger-mediated changes in pH i (HEPES-buffer), and its mechanical counterpart, the slow force response, were evaluated. Furthermore, reactive oxygen species production in response to a low concentration of angiotensin II (1.0 nmol/L) or an equipotent concentration of epidermal growth factor (0.1 μg/mL) was compared in myocardial tissue slices from both groups. Compared with scramble, animals transduced with l-shMR showed (1) reduced cardiac MR expression, (2) cancellation of angiotensin II-induced reactive oxygen species production but preservation of epidermal growth factor-induced reactive oxygen species production, (3) cancellation of stretch-triggered increase in ERK1/2-p90 RSK phosphorylation, (4)

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Section: Resultsmentioning

confidence: 99%

Myocardial Mineralocorticoid Receptor Activation by Stretching and Its Functional Consequences

et al. 2014

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“…We have obtained evidence to propose that the SFR is the mechanical expression of a stretch-triggered autocrine/paracrine loop of intracellular signals that involves an increased production of ROS, activation of the redox-sensitive kinase cascade of MEK-ERK1/2-p90RSK, and the consequent phosphorylation (activation) of the cardiac Na ϩ /H ϩ exchanger (NHE1) (for review see Ref. 23). …”

Section: The Anrep Effect: a Redox-sensitive Phenomenon (Presented Bymentioning

confidence: 99%

Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses

Chatterjee

Fujiwara

Pérez

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Chatterjee S, Fujiwara K, Pérez NG, Ushio-Fukai M, Fisher AB. Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses. Am J Physiol Heart Circ Physiol 308: H1451-H1462, 2015. First published April 10, 2015; doi:10.1152/ajpheart.00105.2015.-Cells are constantly exposed to mechanical forces that play a role in modulating cellular structure and function. The cardiovascular system experiences physical forces in the form of shear stress and stretch associated with blood flow and contraction, respectively. These forces are sensed by endothelial cells and cardiomyocytes and lead to responses that control vascular and cardiac homeostasis. This was highlighted at the Pan American Physiological Society meeting at Iguassu Falls, Brazil, in a symposium titled "Mechanosignaling in the Vasculature." This symposium presented recent research that showed the existence of a vital link between mechanosensing and downstream redox sensitive signaling cascades. This link helps to transduce and transmit the physical force into an observable physiological response. The speakers showcased how mechanosensors such as ion channels, membrane receptor kinases, adhesion molecules, and other cellular components transduce the force via redox signals (such as reactive oxygen species and nitric oxide) to receptors (transcription factors, growth factors, etc.). Receptor activated pathways then lead to cellular responses including cellular proliferation, contraction, and remodeling. These responses have major relevance to the physiology and pathophysiology of various cardiovascular diseases. Thus an understanding of the complex series of events, from the initial sensing through the final response, is essential for progress in this field. Overall, this symposium addressed some important emerging concepts in the field of mechanosignaling and the eventual pathophysiological responses. Anrep effect; mechanotransduction; NADPH oxidase; revascularization; vasculature THIS ARTICLE is part of a collection on 1st PanAmerican Congress of Physiological Sciences: Physiology Without Borders. Other articles appearing in this collection, as well as a full archive of all collections, can be found online at http:// ajpheart.physiology.org/.Cells in vivo are constantly exposed to the physical forces associated with their local environment. Although it was well known that forces such as gravity and friction act on organisms and affect their function and structure, it is only in the last two decades that the complex processes by which these forces are sensed by cells is becoming clear (37,48,55,98). Cells and indeed cellular structures respond to external forces in a manner similar to chemical signaling where chemicals (ligands) bind to specific receptors on cells and initiate cellular signaling and an eventual response (24,26,36). Likewise, mechanical signaling or mechanotransduction involves the activation of receptors. Analogous to chemical signaling or chemotransduction, physical forces trigger a signaling proces...

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“…Although the Frank-Starling mechanism has been well established for over a century, the molecular mechanisms underlying this phenomenon are not well resolved. At the cellular level, a sustained increase in sarcomere length results in both an immediate and a secondary, slower, increase in twitch force that develops over several minutes (2). The latter phase, termed the slow force response, is caused by an alteration in cardiac myocyte Ca 2ϩ homeostasis induced by a strain-dependent mechanism that, too, is incompletely understood (2).…”

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confidence: 99%

“…At the cellular level, a sustained increase in sarcomere length results in both an immediate and a secondary, slower, increase in twitch force that develops over several minutes (2). The latter phase, termed the slow force response, is caused by an alteration in cardiac myocyte Ca 2ϩ homeostasis induced by a strain-dependent mechanism that, too, is incompletely understood (2). Existing data, mostly derived from permeabilized isolated myocardium, strongly supports the notion that the immediate increase in twitch force development upon stretch is directly due to an increase in the Ca 2ϩ responsiveness of the cardiac contractile apparatus itself (3,4), a phenomenon termed myofilament length-dependent activation (LDA) 2 (1).…”

mentioning

confidence: 99%

Cardiac Myosin-binding Protein C and Troponin-I Phosphorylation Independently Modulate Myofilament Length-dependent Activation

Kumar

Govindan

Zhang

et al. 2015

Journal of Biological Chemistry

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Background: Myofilament length-dependent activation (LDA) is modulated by phosphorylation. Results: Myosin binding protein C (MyBP-C) constitutes the dominant molecular mechanism underlying phosphorylation, with a minor and independent contribution of cardiac troponin-I (cTnI). Conclusion: MyBP-C, and to a lesser extent cTnI, both contribute to enhance LDA. Significance: Novel insights into the molecular basis LDA and its regulation by phosphorylation.

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The Anrep effect: 100 years later

Cited by 137 publications

References 81 publications

Myocardial Mineralocorticoid Receptor Activation by Stretching and Its Functional Consequences

Myocardial Mineralocorticoid Receptor Activation by Stretching and Its Functional Consequences

Mechanosignaling in the vasculature: emerging concepts in sensing, transduction and physiological responses

Cardiac Myosin-binding Protein C and Troponin-I Phosphorylation Independently Modulate Myofilament Length-dependent Activation

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