Spinal cord injury blunted effects of endothelin-1 on Ca(2+) transients and calcium current in isolated rat cardiomyocytes.

Plasma endothelin-1 (ET-1) levels are elevated in spinal cord injury (SCI), and ET-1 may be involved in the pathophysiology of this condition. However, its effects on contractile function of the heart of SCI rats are still unknown. To define more clearly the possible role of ET-1 following SCI, we investigated the effect of ET-1 on the contraction, calcium transients and L-type calcium current (I(Ca,L)) in the cardiomyocytes of control and SCI rats. Sixteen Sprague-Dawley male rats aged 80-100 days and weighing 250-350 g were randomized into control and SCI groups. Fourteen days following compression injury to the spinal cord, effects of ET-1 on the contraction, calcium transients and I(Ca,L) were studied in the cardiomyocytes of control and SCI rats by the technique of simultaneous measurement of intracellular Ca(2+) and contraction and by whole-cell configuration of the patch-clamp technique. In myocytes from control rats, ET-1 significantly increased contraction, the magnitude of Ca(2+) transients and the peak amplitude of I(Ca,L). However, ET-1 had little effect on the amplitude of contraction, calcium transients and I(Ca,L). in myocytes from SCI rats. These results suggest that the positive inotropic effects of ET-1 on control myocardial contraction may be altered in pathological states such as SCI.