Search results for: Irene L. Ennis

Items from 1 to 18 out of 18 results

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Nitric oxide and CaMKII: Critical steps in the cardiac contractile response To IGF-1 and swim training

Juan I. Burgos, Alejandra M. Yeves, Jorge P. Barrena, Enrique L. Portiansky, more

Journal of Molecular and Cellular Cardiology > 2017 > 112 > C > 16-26

Cardiac adaptation to endurance training includes improved contractility by a non-yet clarified mechanism. Since IGF-1 is the main mediator of the physiological response to exercise, we explored its effect on cardiac contractility and the putative involvement of nitric oxide (NO) and CaMKII in control and swim-trained mice.IGF-1 increased cardiomyocyte shortening (128.1±4.6% vs. basal; p˂0.05) and...

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Early Hypertrophic Signals After Myocardial Stretch. Role of Reactive Oxygen Species and the Sodium/Hydrogen Exchanger

Horacio E. Cingolani, Néstor G. Pérez, Claudia I. Caldiz, Carolina D. Garciarena, more

Mechanosensitivity in Cells and Tissues > Mechanosensitivity of the Heart > Mechano-Electric Feedback in the Whole Heart and a Computer Simulation Study > 327-371

In this chapter the enhanced activity of the cardiac Na⁺/H⁺ exchanger (NHE-1) after myocardial stretch is considered a key step of the intracellular signaling pathway leading to the slow force response to stretch as well as an early signal for the development of cardiac hypertrophy. We propose that the chain of events triggered by stretch begins with the release of small amounts of angiotensin II...

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Reactive oxygen species partially mediate high dose angiotensin II-induced positive inotropic effect in cat ventricular myocytes

Alejandra M. Yeves, Claudia I. Caldiz, Ernesto A. Aiello, María C. Villa-Abrille, more

Cardiovascular Pathology > 2015 > 24 > 4 > 236-240

Reactive oxygen species, such as superoxide, are being increasingly recognized as key components of a vast array of signaling pathways. Angiotensin II is a well-recognized stimulus for superoxide production through NADPH oxidase activation and opening of the mitochondrial ATP-sensitive potassium channels (mK _ATP ). A role for this mechanism has been proposed to explain several physiological...

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Physiological cardiac hypertrophy: Critical role of AKT in the prevention of NHE-1 hyperactivity

Alejandra M. Yeves, María C. Villa-Abrille, Néstor G. Pérez, Andrés J. Medina, more

Journal of Molecular and Cellular Cardiology > 2014 > 76 > C > 186-195

The involvement of NHE-1 hyperactivity, critical for pathological cardiac hypertrophy (CH), in physiological CH has not been elucidated yet. Stimulation of NHE-1 increases intracellular Na⁺ and Ca²⁺ favouring calcineurin activation. Since myocardial stretch, an activator of NHE-1, is common to both types of CH, we speculate that NHE-1 hyperactivity may also happen in physiological CH. However, calcineurin...

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Endogenous endothelin 1 mediates angiotensin II-induced hypertrophy in electrically paced cardiac myocytes through EGFR transactivation, reactive oxygen species and NHE-1

María V. Correa, Mariela B. Nolly, Claudia I. Caldiz, Gladys E. Chiappe Cingolani, more

Pflügers Archiv - European Journal of Physiology > 2014 > 466 > 9 > 1819-1830

Emerging evidence supports a key role for endothelin-1 (ET-1) and the transactivation of the epidermal growth factor receptor (EGFR) in angiotensin II (Ang II) action. We aim to determine the potential role played by endogenous ET-1, EGFR transactivation and redox-dependent sodium hydrogen exchanger-1 (NHE-1) activation in the hypertrophic response to Ang II of cardiac myocytes. Electrically paced...

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Inappropriate Left Ventricular Mass in a Young Population

Eduardo M. Escudero, Oscar A. Pinilla, Irene L. Ennis

Revista Espanola de Cardiologia (English Edition) > 2012 > 65 > 9 > 855-856

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Sex-Related Difference in Left Ventricular Mass in Nonhypertensive Young Adults: Role of Arterial Pressure

Eduardo M. Escudero, Oscar A. Pinilla, Martín R. Salazar, Irene L. Ennis

Canadian Journal of Cardiology > 2012 > 28 > 4 > 464-470

Blood pressure (BP) is higher in men than in women at similar ages through adult life. Interestingly, a similar pattern is detected in left ventricular mass (LVM), classically attributed to differences in body size. However, the existing difference in BP between sexes might be relevant in determining LVM and it has been not fully investigated. Therefore, we set out to determine the impact of nonhypertensive...

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Mineralocorticoid receptor activation is crucial in the signalling pathway leading to the Anrep effect

Claudia I. Caldiz, Romina G. Díaz, Mariela B. Nolly, Gladys E. Chiappe de Cingolani, more

The Journal of Physiology > 589 > 24 > 6051 - 6061

Non‐technical summary Myocardial stretch increases force in two phases. The first one is immediate and attributed to an increase in myofilament Ca²⁺ responsiveness (Frank–Starling mechanism). The second phase gradually develops and is known as slow force response (SFR) or Anrep effect due to an increase in intracellular Ca²⁺ transient. We previously showed that Ca²⁺ entry through reverse Na⁺/Ca²⁺...

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Role of autocrine/paracrine mechanisms in response to myocardial strain

Horacio E. Cingolani, Irene L. Ennis, Ernesto A. Aiello, Néstor G. Pérez

Pflügers Archiv - European Journal of Physiology > 2011 > 462 > 1 > 29-38

Myocardial strain triggers an autocrine/paracrine mechanism known to participate in myocardial hypertrophy development. After the onset of stretch, there is a rapid augmentation in developed tension due to an increase in myofilament calcium sensitivity (the Frank Starling mechanism) followed by a gradual increase in tension over the next 10–15 min. This second phase is called the slow force response...

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In vivo key role of reactive oxygen species and NHE-1 activation in determining excessive cardiac hypertrophy

Oscar H. Cingolani, Néstor G. Pérez, Irene L. Ennis, María C. Álvarez, more

Pflügers Archiv - European Journal of Physiology > 2011 > 462 > 5 > 733-743

Growing in vitro evidence suggests NHE-1, a known target for reactive oxygen species (ROS), as a key mediator in cardiac hypertrophy (CH). Moreover, NHE-1 inhibition was shown effective in preventing CH and failure; so has been the case for AT1 receptor (AT1R) blockers. Previous experiments indicate that myocardial stretch promotes angiotensin II release and post-translational NHE-1 activation; however,...

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The Anrep effect requires transactivation of the epidermal growth factor receptor

María C. Villa‐Abrille, Claudia I. Caldiz, Irene L. Ennis, Mariela B. Nolly, more

The Journal of Physiology > 588 > 9 > 1579 - 1590

Myocardial stretch elicits a biphasic contractile response: the Frank–Starling mechanism followed by the slow force response (SFR) or Anrep effect. In this study we hypothesized that the SFR depends on epidermal growth factor receptor (EGFR) transactivation after the myocardial stretch‐induced angiotensin II (Ang II)/endothelin (ET) release. Experiments were performed in isolated cat papillary muscles...

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Endothelin-1 induced hypertrophic effect in neonatal rat cardiomyocytes: Involvement of Na+/H+ and Na+/Ca2+ exchangers

Raúl A. Dulce, Cecilia Hurtado, Irene L. Ennis, Carolina D. Garciarena, more

Journal of Molecular and Cellular Cardiology > 2006 > 41 > 5 > 807-815

Endothelin-1 (ET-1) is a potent agonist of cell growth that also stimulates Na ⁺ /H ⁺ exchanger isoform 1 (NHE-1) activity. It was hypothesized that the increase in intracellular Na ⁺ ([Na ⁺ ] _i ) mediated by NHE-1 activity may induce the reverse mode of Na ⁺ /Ca ²⁺ exchanger (NCX _rev ) increasing intracellular Ca ²⁺ ([Ca ...

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Involvement of AE3 isoform of Na+-independent Cl−/HCO3− exchanger in myocardial pHi recovery from intracellular alkalization

Gladys E. Chiappe de Cingolani, Irene L. Ennis, Patricio E. Morgan, Bernardo V. Alvarez, more

Life Sciences > 2006 > 78 > 26 > 3018-3026

Myocardial pH _i recovery from intracellular alkalization results in part from the acid load (−J _H+ ) carried by Cl ⁻ /HCO ₃ ⁻ anion-exchangers (AE). Three AE isoforms, AE1, AE2 and AE3, have been identified in cardiac membranes, but the function of each isoform on pH _i homeostasis is still under investigation. This work explored, by means of specific antibodies,...

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Novel Interactions Identified between μ-Conotoxin and the Na+ Channel Domain I P-loop: Implications for Toxin-Pore Binding Geometry

Tian Xue, Irene L. Ennis, Kazuki Sato, Robert J. French, more

Biophysical Journal > 2003 > 85 > 4 > 2299-2310

μ-Conotoxins (μ-CTX) are peptides that inhibit Na⁺ flux by blocking the Na⁺ channel pore. Toxin residue arginine 13 is critical for both high affinity binding and for complete block of the single channel current, prompting the simple conventional view that residue 13 (R13) leads toxin docking by entering the channel along the pore axis. To date, the strongest interactions identified are between μ-CTX...

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Upregulation of Myocardial Na+/H+ Exchanger Induced by Chronic Treatment with a Selective Inhibitor

Marı́a C. Camilión de Hurtado, Irene L. Ennis, Néstor G. Pérez, Gladys E. Chiappe de Cingolani, more

Journal of Molecular and Cellular Cardiology > 2002 > 34 > 11 > 1539-1547

M. C. Camilión de Hurtad, I. L. Ennis, N. G. Pérez, G. E. C.de Cingolani, P. Morgan and H. E. Cingolani. Upregulation of Myocardial Na ⁺ /H ⁺ Exchanger Induced by Chronic Treatment with a Selective Inhibitor. Journal of Molecular and Cellular Cardiology (2002) 34, 1539–1547. Rats exposed to prolonged administration of the NHE-1 inhibitor cariporide showed enhanced activity of the exchanger...