Antibodies and Autoantibodies Against ADP/ATP Carrier Enhance Calcium Current in Isolated Ventricular Myocytes
Abnormalities in Ca2+ metabolism of myocardium and coronary vessels are thought to be involved in genesis of cardiac myopathies . In Syrian hamster (Bio 14.6), Ca2+ influx was enhanced and Dihydropytidine (DHP) binding sites increased in early stages of cardiac myopathy [4, 10, 12]. Prolongation of action potential reported in cardiomyopathic hamsters  is also consistent with possible enhancement of Ca2+ current. Abnormalities in Ca2+ metabolism may also result from heart reactive antibodies. Such antibodies have been identified in myocarditis and cardiac myopathies [1, 3]. Antibodies previously described as inhibiting the adenosine diphosphate (ADP)/adenosine triphosphate (ATP) carrier of the inner mitochondrial membrane  have been found in myocarditis and dilated cardiomyopathy . Such antibodies were found to bind specifically to the sarcolemma of isolated cardiac myocytes causing oscillating contractions leading to cell death. Cell deterioration, as judged by the number of cells losing their rectangular shape and clear striation, was delayed or prevented by addition of Ca2+ channel blockers to the antibody- containing solutions. These results, consistent with those described in Syrian hamster, suggest that etiology of disease may be related to possible enhancement of the Ca2+ channel, causing subsequent Ca2+ overload. In this report, therefore, we examine the direct effects of antibodies against ADP/ATP carrier and autoantibodies from patients with myocarditis and dilated cardiomyopathies on the Ca2+ current recorded in isolated mammalian and amphibian ventricular myocytes.
KeywordsAdenosine Cardiomyopathy HEPES Cardiol Propranolol
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