Cardiomyopathy is a common, life-threatening, but poorly understood complication of HIV infection. The purpose of the present study is to study the effects of an HIV surface envelope protein, glycoprotein 120 (gp120), on cell contraction and L-type Ca(2+) current in rabbit ventricular myocytes. Rabbit ventricular cells were isolated by an enzyme dissociation method. Cell contractions were induced by electric field stimulation. Whole cell L-type Ca(2+) channel currents were measured by the whole cell voltage-clamp technique. We found that perfusion with solution containing gp120 (0.1 microg/ml) derived from HIV-1(SF2) significantly inhibited field-stimulated contractions and L-type Ca(2+) current in rabbit ventricular myocytes as compared with perfusion with buffer alone. These results suggest that HIV-1 gp120 may directly contribute to cardiac dysfunction as seen in many HIV patients.
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