Objective: To investigate differences between store-dependent Ca2+ in African American and white men.
Method: Thapsigargin, a potent and specific inhibitor of the sarco(endo)plasmic reticulum Ca(2+)-ATPase, was used as a probe to elicit store-dependent Ca2+ fluxes. Treatment with this agent caused a rise in the cytosolic free Ca2+ due to the egress of Ca2+ from thapsigargin-sensitive Ca2+ stores and the acceleration of external Ca2+ influx through store-dependent Ca2+ channels.
Design: Lymphocytes were obtained from 22 African Americans and 23 whites. These cells were subjected to thapsigargin treatment and changes in the cellular Ca2+ profiles were monitored.
Results: Both in Ca(2+)-free and in Ca(2+)-containing media the increases in cytosolic free Ca2+ concentrations after thapsigargin treatment were greater in lymphocytes from African Americans than they were in those from whites. The greater levels of cytosolic Ca2+ concentration were coupled with higher rates of Ca2+ extrusion in thapsigargin-treated lymphocytes from African Americans.
Conclusions: These findings suggest that store-dependent Ca2+ fluxes are greater in lymphocytes from African Americans than they are in those from whites. This phenomenon increases the Ca2+ turnover rate and might augment the sensitivity to agonists acting through Ca2+ signaling systems, thereby predisposing African Americans to essential hypertension.