Chromium picolinate modulates rat vascular smooth muscle cell intracellular calcium metabolism.

We have previously shown that insulin attenuates vasoconstriction, accelerates both vascular relaxation and [Ca2+]i recovery from pressor agonist-induced Ca2+ loads, and stimulates Ca2+-ATPase gene expression in rat and human vascular smooth muscle cells (VSMC). Moreover, these functions are impaired in VSMC from both insulin resistant and insulinopenic rats, suggesting that hypertension in insulin resistant states may result, in part, from impaired insulin-regulation of VSMC Ca2+ transport. Accordingly, we have now evaluated the effect of improving cellular insulin sensitivity with chromium picolinate (CrPic) on regulation of VSMC Ca2+ transport. Cultured VSMC from rats were grown from passage to confluence in the presence or absence of 1 micromol/L CrPic, maintained in a quiescent medium for 24 h and incubated with or without insulin (10(-8) mol/L) for the final 2 h. Cells were then harvested and RNA and protein extracted for Northern and Western blot analysis, respectively. Insulin caused a significant stimulation of plasmalemmal Ca2+-ATPase mRNA and protein (P < 0.05). A comparable stimulation of the mRNA and protein levels was caused by CrPic in the absence of insulin (P < 0.05), while the CrPic + insulin treatment caused a greater percentage stimulation of the Ca2+-ATPase mRNA level than either separate treatment (P < 0.05). Fluorometric analysis of the rate of [Ca2+]i recovery following stimulation with arginine vasopressin support these findings: insulin caused an 83% increase, CrPic caused a 35% increase and insulin + CrPic caused a 133% increase in [Ca2+]i recovery rate. These data suggest that CrPic may be an effective modality to reduce VSMC [Ca2+]i loads and thereby reduce peripheral vascular resistance in insulin resistant states.