Previous studies have shown that high glucose concentrations alter membrane cation permeability and contractile responses of vascular smooth muscle. We determined whether 12 weeks of diabetes alters Ca influx via voltage-gated Ca channels (VGCC). Whole-cell VGCC currents were measured with the perforated-patch technique in epicardial coronary smooth musde cells from control and diabetic pigs. Cells from both groups exhibited only L-type Ca current. Current density was smaller in cells from diabetic pigs (maximal density: 1.93 ±0.42 pA/pF vs. 1.18±0.15 pA/pF, p<0 05, n=19-36). The current-voltage relationships and steady-state inactivation curves were similar between control and diabetic pigs. The VGCC agonist, Bay K 8644 (1-100 nM), increased the current up to 4-fold in both groups with no difference in concentration dependence. Inactivation curves in the presence of Bay K 8844 were also similar between control and diabetic pigs. However, the leftward shift of the current-voltage relationships induced by Bay K 8644 (10nM and 100 nM) was greater in cells from diabetic pigs. These results indicate that VGCC may be altered in diabetes and this change may partly underiy abnormal smooth muscle function in diabetes. (Supported by an ADA grant; NIH grant RCDA HL02872; and pre- and postdoctoral fellowships from AHA, MO-Affiliate).
|Original language||English (US)|
|State||Published - Dec 1 1996|
ASJC Scopus subject areas
- Molecular Biology