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Néstor G. Pérez

Researcher at National University of La Plata

Publications -  71
Citations -  2997

Néstor G. Pérez is an academic researcher from National University of La Plata. The author has contributed to research in topics: Angiotensin II & Sodium–hydrogen antiporter. The author has an hindex of 30, co-authored 69 publications receiving 2869 citations. Previous affiliations of Néstor G. Pérez include National Scientific and Technical Research Council & Johns Hopkins University.

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Role of Troponin I Proteolysis in the Pathogenesis of Stunned Myocardium

TL;DR: The results show that TnI is partially and selectively degraded in stunned myocardium; this degradation could be prevented by low Ca2+/low pH reperfusion, which also prevented the contractile dysfunction of stunning; and calpain I could similarly degrade Tni, supporting the idea that Ca(2+)-dependent myofilament proteolysis underlies myocardial stunning.
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Mechanisms Underlying the Increase in Force and Ca2+ Transient That Follow Stretch of Cardiac Muscle A Possible Explanation of the Anrep Effect

TL;DR: The data indicate that the second force phase and the increase in [Ca(2+)](i) transient after stretch result from activation of the Na(+)/H(+) exchanger (NHE) increasing [Na(+)] (i) and leading to a secondary increase in [/Ca( 2+](i), which reflects an autocrine-paracrine mechanism.
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Reverse Mode of the Na+-Ca2+ Exchange After Myocardial Stretch : Underlying Mechanism of the Slow Force Response

TL;DR: Evidence is provided that the last step of the autocrine-paracrine mechanism leading to the SFR to stretch is Ca2+ entry through the reverse mode of Na+-Ca2+ exchange.
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The Anrep effect: 100 years later.

TL;DR: The experimental evidence supporting each of the signaling steps leading to the Anrep effect and its blunting is presented by silencing NHE1 expression with a specific small hairpin interference RNA injected into the ventricular wall.
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Calcium cycling and contractile activation in intact mouse cardiac muscle

TL;DR: The strong positive force‐frequency relationship in mouse cardiac muscle, with increases of force disproportionate to the increases in Ca2+ transients, suggests frequency‐dependent ‘sensitization’ of the myofilaments.