Protein restriction after weaning modifies the calcium kinetics and induces cardiomyocyte contractile dysfunction in rats.
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Date
2013
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Abstract
Protein restriction (PR) is associated with cardiovascular diseases.
The purpose of this study was to investigate the effects
on single ventricular cardiomyocyte contractile function
of a short-term PR after weaning. Male Fischer rats that
were 28 days old were randomly divided into a control group
(CG, n = 16) and a protein-restricted group (PRG, n = 16). After
weaning, CG and PRG animals received isocaloric diets
containing 15 and 6% protein, respectively, for 35 days. Biometric
parameters were then measured, and the hearts were
removed for the analysis of contractile function and calcium
transient in isolated cardiomyocytes of the left ventricule
(LV), and the quantification of calcium and collagen fibers in
LV myocardium. PRG animals had lower body weight (BW)
and LV weight (LVW), an increased LVW to BW ratio and a
higher proportion of collagen fibers than CG animals. PRG
animals exhibited reduced tissue levels of calcium, reduced
the length, width and volume of cardiomyocytes and their
sarcomere length compared to CG animals. Cardiomyocytes
from PRG animals had a lower amplitude of shortening, a slower time to the peak of shortening and a longer time to
half-relaxation than those from the CG. Cardiomyocytes
from PRG animals also presented a lower peak of calcium
transient and a longer calcium transient decay time than CG
animals. Taken together, the results indicate that short-term
PR after weaning induces a marked structural remodeling of
the myocardium parenchyma and stroma that coexists with
contractile dysfunctions in single LV cardiomyocytes of rats,
which is probably associated with pathological changes of
the intracellular calcium kinetics, rather than inadequate
available amounts of this mineral in cardiac tissue.
Description
Keywords
Malnutrition, Cardiovascular system, Calcium transient
Citation
PENITENTE, A. R. et al. Protein restriction after weaning modifies the calcium kinetics and induces cardiomyocyte contractile dysfunction in rats. Cells Tissues Organs, v. 198, p. 311-317, 2013. Disponível em: <https://www.karger.com/Article/FullText/355943>. Acesso em: 19 fev. 2017.