Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes

In healthy hearts, ventricular ejection is determined by three myofibrillar properties; force, force development rate, and rate of loaded shortening (i.e., power). The sarcomere length and PKA dependence of these mechanical properties were measured in porcine cardiac myocytes. Permeabilized myocytes...

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Main Authors: Kerry S. McDonald, Laurin M. Hanft, Timothy L. Domeier, Craig A. Emter
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Biochemistry Research International
Online Access:http://dx.doi.org/10.1155/2012/371415
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author Kerry S. McDonald
Laurin M. Hanft
Timothy L. Domeier
Craig A. Emter
author_facet Kerry S. McDonald
Laurin M. Hanft
Timothy L. Domeier
Craig A. Emter
author_sort Kerry S. McDonald
collection DOAJ
description In healthy hearts, ventricular ejection is determined by three myofibrillar properties; force, force development rate, and rate of loaded shortening (i.e., power). The sarcomere length and PKA dependence of these mechanical properties were measured in porcine cardiac myocytes. Permeabilized myocytes were prepared from left ventricular free walls and myocyte preparations were calcium activated to yield ~50% maximal force after which isometric force was measured at varied sarcomere lengths. Porcine myocyte preparations exhibited two populations of length-tension relationships, one being shallower than the other. Moreover, myocytes with shallow length-tension relationships displayed steeper relationships following PKA. Sarcomere length-Ktr relationships also were measured and Ktr remained nearly constant over ~2.30 μm to ~1.90 μm and then increased at lengths below 1.90 μm. Loaded-shortening and peak-normalized power output was similar at ~2.30 μm and ~1.90 μm even during activations with the same [Ca2+], implicating a myofibrillar mechanism that sustains myocyte power at lower preloads. PKA increased myocyte power and yielded greater shortening-induced cooperative deactivation in myocytes, which likely provides a myofibrillar mechanism to assist ventricular relaxation. Overall, the bimodal distribution of myocyte length-tension relationships and the PKA-mediated changes in myocyte length-tension and power are likely important modulators of Frank-Starling relationships in mammalian hearts.
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spelling doaj-art-aece3ee099994d6d8a68d783262f5c4c2025-02-03T06:01:14ZengWileyBiochemistry Research International2090-22472090-22552012-01-01201210.1155/2012/371415371415Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac MyocytesKerry S. McDonald0Laurin M. Hanft1Timothy L. Domeier2Craig A. Emter3Department of Medical Pharmacology & Physiology, School of Medicine, University of Missouri, Columbia, MO 65212, USADepartment of Medical Pharmacology & Physiology, School of Medicine, University of Missouri, Columbia, MO 65212, USADepartment of Medical Pharmacology & Physiology, School of Medicine, University of Missouri, Columbia, MO 65212, USADepartment of Biomedical Sciences, College of Veterinary Medicine, University of Missouri, Columbia, MO 65212, USAIn healthy hearts, ventricular ejection is determined by three myofibrillar properties; force, force development rate, and rate of loaded shortening (i.e., power). The sarcomere length and PKA dependence of these mechanical properties were measured in porcine cardiac myocytes. Permeabilized myocytes were prepared from left ventricular free walls and myocyte preparations were calcium activated to yield ~50% maximal force after which isometric force was measured at varied sarcomere lengths. Porcine myocyte preparations exhibited two populations of length-tension relationships, one being shallower than the other. Moreover, myocytes with shallow length-tension relationships displayed steeper relationships following PKA. Sarcomere length-Ktr relationships also were measured and Ktr remained nearly constant over ~2.30 μm to ~1.90 μm and then increased at lengths below 1.90 μm. Loaded-shortening and peak-normalized power output was similar at ~2.30 μm and ~1.90 μm even during activations with the same [Ca2+], implicating a myofibrillar mechanism that sustains myocyte power at lower preloads. PKA increased myocyte power and yielded greater shortening-induced cooperative deactivation in myocytes, which likely provides a myofibrillar mechanism to assist ventricular relaxation. Overall, the bimodal distribution of myocyte length-tension relationships and the PKA-mediated changes in myocyte length-tension and power are likely important modulators of Frank-Starling relationships in mammalian hearts.http://dx.doi.org/10.1155/2012/371415
spellingShingle Kerry S. McDonald
Laurin M. Hanft
Timothy L. Domeier
Craig A. Emter
Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
Biochemistry Research International
title Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
title_full Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
title_fullStr Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
title_full_unstemmed Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
title_short Length and PKA Dependence of Force Generation and Loaded Shortening in Porcine Cardiac Myocytes
title_sort length and pka dependence of force generation and loaded shortening in porcine cardiac myocytes
url http://dx.doi.org/10.1155/2012/371415
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