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Does an impaired adenosine mediated feedback control play a role in the development of hereditary dystrophic
Insights
This study found that adenosine
Area of Science:
- Cardiology
- Molecular Biology
- Genetics
Background:
- Hereditary cardiomyopathy in Syrian hamsters is a model for human heart disease.
- The role of adenosine in cardiac function during disease progression is not fully understood.
Purpose of the Study:
- To investigate the role of adenosine-mediated negative inotropic effects in the pathogenesis of hereditary cardiomyopathy.
- To determine if impaired adenosine feedback control contributes to heart dysfunction in Syrian hamsters.
Main Methods:
- Papillary muscles from cardiomyopathic and control Syrian hamsters were isolated.
- The effects of isoprenaline and adenosine on muscle contraction were measured.
- Experiments were conducted during the prenecrotic stage of the disease.
Main Results:
- Adenosine antagonized the positive inotropic effect of isoprenaline in both cardiomyopathic and control hamsters.
- Adenosine alone had minimal inhibitory effects on contraction force.
- The effects of adenosine and isoprenaline did not differ between cardiomyopathic and control groups.
Conclusions:
- Adenosine's feedback control of the heart is not impaired in this model of hereditary cardiomyopathy.
- Impaired adenosine function does not appear to play a role in the pathogenesis of this specific cardiac disorder.
Abstract:
A study was carried out to investigate whether or not an impairment of the adenosine mediated negative inotropic effect in the presence of beta adrenoceptor stimulation plays a role in the pathogenesis of the hereditary cardiomyopathy of the Syrian hamster. In electrically driven papillary muscles isolated from the hearts of cardiomyopathic (strain BIO 8262) and age matched healthy control Syrian hamsters the effects of isoprenaline, adenosine, and adenosine in the presence of isoprenaline were studied within the first 30 days of life (the prenecrotic stage of the disorder). In both cardiomyopathic and control hamsters adenosine antagonised the positive inotropic effect of isoprenaline, whereas adenosine alone had no or, only a weak, inhibitory effect on the force of contraction. The effects in both groups were similar. The effect of isoprenaline on the force of contraction also did not differ in the two groups. The data show that in both cardiomyopathic and control hamsters adenosine reduces the force of contraction during beta adrenergic stimulation. The potency or efficacy of adenosine did not differ in the two groups. An impaired adenosine mediated feedback control of the heart does not therefore seem to play a role in the pathogenesis of the hereditary dystrophic cardiomyopathy of the Syrian hamster.