Overexpression of neuronal calcium sensor‐1 alters contractile function in adult rat ventricular myocytes

Abstract

Neuronal-calcium sensor-1 (NCS-1), a small calcium binding protein, has been shown to interact with ion channels (including Ca channels) in neuronal cells. We have previously reported that NCS-1 was also present in rat cardiomyocytes. The present study examined whether NCS-1 overexpression in ventricular myocytes alters the contractile function. Isolated adult rat ventricular myocytes were infected with an adenovirus construct expressing NCS-1 (MOI: 100). At 48 hours after infection, myocytes were rinsed with control culture medium, and cell shortening was elicited in normal Tyrode's solution with field stimulation. The kinetics of steady-state cell shortening and the post-rest potentiation were monitored, and compared with those of non-infected time-control myocytes. Our results show that the rise time (10–90% of time-to-peak) and half-width (50% of duration) of cell shortening in NCS-1-infected cells were significantly reduced (31.1±0.9 and 57.3±2.3 ms vs. 37.5±1.5 and 68.7±2.8 ms in control cells, respectively, n=23 from 5 hearts). However, the decay time (10–90% of relaxation) was not significantly altered in the NCS-1-infected cells. Post-rest potentiation in NCS-1 cells was significantly increased after a 60-sec rest period (P=0.037, n=18), but not after a 30-sec rest (P=0.076, n=22). Taken together, our data suggest that NCS-1 alters the contractile function by facilitating contraction, with a slight alteration of sarcoplasmic reticular function in adult rat ventricular myocytes.