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Short-term effects of β 2-AR blocker ICI 118,551 on sarcoplasmic reticulum SERCA2a and cardiac function of rats with heart failure

View Article: PubMed Central - PubMed

ABSTRACT

The study was conducted to examine the effects of ICI 118,551 on the systolic function of cardiac muscle cells of rats in heart failure and determine the molecular mechanism of selective β2-adrenergic receptor (β2-AR) antagonist on these cells. The chronic heart failure model for rats was prepared through abdominal aortic constriction and separate cardiac muscle cells using the collagenase digestion method. The rats were then divided into Sham, HF and HF+ICI 50 nM goups and cultivated for 48 h. β2-AR, Gi/Gs and sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) protein expression levels in the cardiac muscle cells were evaluated by western blotting and changes in the systolic function of cardiac muscle cells based on the boundary detection system of contraction dynamics for individual cells was measured. The results showed that compared with the Sham group, the survival rate, percentage of basic contraction and maximum contraction amplitude percentage of cardiac muscle cells with heart failure decreased, Gi protein expression increased while Gs and SERCA2a protein expression decreased. Compared with the HF group, the maximum contraction amplitude percentage of cardiac muscle cells in group HF+ICI 50 nM decreased, the Gi protein expression level increased while the SERCA2a protein expression level decreased. Following the stimulation of Ca2+ and ISO, the maximum contraction amplitude percentage of cardiac muscle cells in the HF+ICI 50 nM group was lower than that in group HF. This indicated that ICI 118,551 has negative inotropic effects on cardiac muscle cells with heart failure, which may be related to Gi protein. Systolic function of cardiac muscle cells with heart failure can therefore be reduced by increasing Gi protein expression and lowering SERCA2a protein expression.

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Protein expression of β2-AR, Gi, Gs and SERCA2a of rats with heart failure in the various groups. Compared with the Sham group, *P<0.05; compared with group HF, ▽P<0.05. β2-AR, β2-adrenergic receptor; SERCA2a, sarcoplasmic reticulum Ca2+-ATPase; HF, heart failure.
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f3-etm-0-0-3450: Protein expression of β2-AR, Gi, Gs and SERCA2a of rats with heart failure in the various groups. Compared with the Sham group, *P<0.05; compared with group HF, ▽P<0.05. β2-AR, β2-adrenergic receptor; SERCA2a, sarcoplasmic reticulum Ca2+-ATPase; HF, heart failure.

Mentions: Compared with the Sham group, Gi protein expression levels in group HF and HF+ICI 50 nM increased (P<0.05), whereas Gs protein expression (P<0.05) and SERCA2a protein expression (P<0.05) decreased. Compared with group HF, there were no obvious differences in terms of β2-AR protein and Gs protein expression amounts for cardiac muscle cells in group HF+ICI 50 nM (P>0.05). Gi protein expression increased (P<0.05) but the SERCA2a protein expression amount was obviously decreased (P<0.05) (Fig. 3).


Short-term effects of β 2-AR blocker ICI 118,551 on sarcoplasmic reticulum SERCA2a and cardiac function of rats with heart failure
Protein expression of β2-AR, Gi, Gs and SERCA2a of rats with heart failure in the various groups. Compared with the Sham group, *P<0.05; compared with group HF, ▽P<0.05. β2-AR, β2-adrenergic receptor; SERCA2a, sarcoplasmic reticulum Ca2+-ATPase; HF, heart failure.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4998176&req=5

f3-etm-0-0-3450: Protein expression of β2-AR, Gi, Gs and SERCA2a of rats with heart failure in the various groups. Compared with the Sham group, *P<0.05; compared with group HF, ▽P<0.05. β2-AR, β2-adrenergic receptor; SERCA2a, sarcoplasmic reticulum Ca2+-ATPase; HF, heart failure.
Mentions: Compared with the Sham group, Gi protein expression levels in group HF and HF+ICI 50 nM increased (P<0.05), whereas Gs protein expression (P<0.05) and SERCA2a protein expression (P<0.05) decreased. Compared with group HF, there were no obvious differences in terms of β2-AR protein and Gs protein expression amounts for cardiac muscle cells in group HF+ICI 50 nM (P>0.05). Gi protein expression increased (P<0.05) but the SERCA2a protein expression amount was obviously decreased (P<0.05) (Fig. 3).

View Article: PubMed Central - PubMed

ABSTRACT

The study was conducted to examine the effects of ICI 118,551 on the systolic function of cardiac muscle cells of rats in heart failure and determine the molecular mechanism of selective &beta;2-adrenergic receptor (&beta;2-AR) antagonist on these cells. The chronic heart failure model for rats was prepared through abdominal aortic constriction and separate cardiac muscle cells using the collagenase digestion method. The rats were then divided into Sham, HF and HF+ICI 50 nM goups and cultivated for 48 h. &beta;2-AR, Gi/Gs and sarcoplasmic reticulum Ca2+-ATPase (SERCA2a) protein expression levels in the cardiac muscle cells were evaluated by western blotting and changes in the systolic function of cardiac muscle cells based on the boundary detection system of contraction dynamics for individual cells was measured. The results showed that compared with the Sham group, the survival rate, percentage of basic contraction and maximum contraction amplitude percentage of cardiac muscle cells with heart failure decreased, Gi protein expression increased while Gs and SERCA2a protein expression decreased. Compared with the HF group, the maximum contraction amplitude percentage of cardiac muscle cells in group HF+ICI 50 nM decreased, the Gi protein expression level increased while the SERCA2a protein expression level decreased. Following the stimulation of Ca2+ and ISO, the maximum contraction amplitude percentage of cardiac muscle cells in the HF+ICI 50 nM group was lower than that in group HF. This indicated that ICI 118,551 has negative inotropic effects on cardiac muscle cells with heart failure, which may be related to Gi protein. Systolic function of cardiac muscle cells with heart failure can therefore be reduced by increasing Gi protein expression and lowering SERCA2a protein expression.

No MeSH data available.


Related in: MedlinePlus