NDLI: Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.

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Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.

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Sarcomeric protein modification during adrenergic stress enhances cross-bridge kinetics and cardiac output.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gresham, Kenneth S. Mamidi, Ranganath Li, Jiayang Kwak, Hyerin Stelzer, Julian E.
Description	Author Affiliation: Gresham KS ( Case Western Reserve University.); Mamidi R ( Case Western Reserve University.); Li J ( Case Western Reserve University.); Kwak H ( Case Western Reserve University.); Stelzer JE ( Department of Physiology and Biophysics, School of Medicine, Case Western Reserve University, Cleveland, OH 44106 julian.stelzer@case.edu.)
Abstract	Molecular adaptations to chronic neurohormonal stress, including sarcomeric protein cleavage and phosphorylation, provide a mechanism to increase ventricular contractility and enhance cardiac output, yet the link between sarcomeric protein modifications and changes in myocardial function remains unclear. To examine the effects of neurohormonal stress on post-translational modifications of sarcomeric proteins, mice were administered combined - and ß-adrenergic receptor agonists (isoproterenol and phenylephrine; IPE) for 14 days using implantable osmotic pumps. In addition to significant cardiac hypertrophy and increased maximal ventricular pressure, IPE treatment accelerated pressure development and relaxation (74% increase in dp/dt and 14% decrease in τ) resulting in a 52% increase in cardiac output compared to saline (SAL) treated mice. Accelerated pressure development was maintained when accounting for changes in heart rate and preload, suggesting that myocardial adaptations contribute to enhanced ventricular contractility. Ventricular myocardium isolated from IPE-treated mice displayed a significant reduction in troponin I (TnI) and myosin binding protein-c (MyBP-C) expression and a concomitant increase in the phosphorylation levels of the remaining TnI and MyBP-C protein compared to myocardium isolated from saline-treated control mice. Skinned myocardium isolated from IPE treated mice displayed a significant acceleration in the rate of cross-bridge (XB) detachment (46% increase) and an enhanced magnitude of XB recruitment (43% increase) at submaximal Ca activation compared to SAL treated mice, but unaltered myofilament Ca sensitivity of force generation. These findings demonstrate that sarcomeric protein modifications during neurohormonal stress are molecular adaptations that enhance in vivo ventricular contractility through accelerated XB kinetics to increase cardiac output.
File Format	HTM / HTML
ISSN	87507587
e-ISSN	15221601
Journal	Journal of Applied Physiology
Language	English
Publisher	American Physiological Society
Publisher Date	2016-12-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Applied Physiology Molecular Biology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Physiology Physiology (medical) Sports Science

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