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Published on: December 22, 2020
Load-dependent effects of apelin on murine cardiomyocytes
Rémi Peyronnet1, Christian Bollensdorff2, Rebecca A Capel3
1Institute for Experimental Cardiovascular Medicine, University Heart Centre Freiburg · Bad Krozingen, Medical School of the University of Freiburg, Germany; Imperial College London, NHLI, Heart Science Centre, UK.
Insights
Apelin peptide enhances cardiac relaxation (lusitropy) in single cardiomyocytes, a finding observed in apelin-deficient models. This preload-dependent effect may explain apelin
Area of Science:
- Cardiology
- Molecular Biology
- Physiology
Background:
- Apelin peptide is a potent endogenous inotropic agent found in cardiomyocytes.
- Apelin's cellular-level effects and mechanisms on cardiac function remain unclear.
- Previous studies suggest cardio-protective roles and positive effects on contractility.
Purpose of the Study:
- To investigate the effects of apelin on the dynamic mechanical properties of single ventricular cardiomyocytes.
- To elucidate the cellular mechanisms underlying apelin's influence on cardiac contractility and relaxation.
Main Methods:
- Studied single ventricular cardiomyocytes from control, Apelin-KO, and APJ-KO mice, and rats.
- Measured dynamic changes in cell shortening and relaxation velocities.
- Utilized the carbon fiber technique to assess cell shortening and peak force development under varying preloads.
Main Results:
- Apelin (10 nM) demonstrated a preload-dependent reduction in the end-diastolic stress-length relation slope in Apelin-KO cardiomyocytes.
- This indicates a positive lusitropic effect (enhanced relaxation) of apelin.
- The observed lusitropy may reconcile previous findings of increased contractility without elevated oxygen consumption.
Conclusions:
- Apelin exerts a significant positive lusitropic effect on cardiomyocytes.
- This finding provides a cellular mechanism for apelin's impact on cardiac function.
- Apelin's role in cardiac relaxation warrants further investigation for therapeutic potential.
Abstract:
The apelin peptide is described as one of the most potent inotropic agents, produced endogenously in a wide range of cells, including cardiomyocytes. Despite positive effects on cardiac contractility in multicellular preparations, as well as indications of cardio-protective actions in several diseases, its effects and mechanisms of action at the cellular level are incompletely understood. Here, we report apelin effects on dynamic mechanical characteristics of single ventricular cardiomyocytes, isolated from mouse models (control, apelin-deficient [Apelin-KO], apelin-receptor KO mouse [APJ-KO]), and rat. Dynamic changes in maximal velocity of cell shortening and relaxation were monitored. In addition, more traditional indicators of inotropic effects, such as maximum shortening (in mechanically unloaded cells) or peak force development (in auxotonic contracting cells, preloaded using the carbon fibre technique) were studied. The key finding is that, using Apelin-KO cardiomyocytes exposed to different preloads with the 2-carbon fibre technique, we observe a lowering of the slope of the end-diastolic stress-length relation in response to 10 nM apelin, an effect that is preload-dependent. This suggests a positive lusitropic effect of apelin, which could explain earlier counter-intuitive findings on an apelin-induced increase in contractility occurring without matching rise in oxygen consumption.
