Effects of vanadate, menadione and menadione analogs on the Ca2+-activated K+ channels in human red cells. Possible relations to membrane-bound oxidoreductase activity

Potassium channel modulation in rat portal vein by ATP depletion: a comparison with the effects of levcromakalim (BRL 38227)

“…To ensure that the results were comparable with those of our earlier studies (Noack et al, 1992a,b), Ca-free conditions together with EGTA buffering were used. Such conditions also minimize the possibility of Ca-overloading due to loss of mitochondrial calcium and failure of Ca-pumping which can occur in the absence of intracellular ATP (Fuhrmann et al, 1985;Klockner & Isenberg, 1992).…”

Endothelin‐1 receptor antagonists regulate cell surface‐associated protein disulfide isomerase in sickle cell disease

“…There is evidence of abnormal redox status in sRBCs (13). Modification of plasma membrane redox status has been shown to regulate erythrocyte K + transport and hydration status through mechanisms not clearly described (49). We now report on the presence of the thiol/disulfide interchange enzyme, PDI, in human and mouse erythrocytes and that blockade of its activity leads to reduced Gardos channel activity and modulation of sickle erythrocyte hydration status.…”

Properties of the Ca2+ influx reveal the duality of events underlying the activation by vanadate and fluoride of the Gárdos effect in human red blood cells

“…A feature of the Gárdos effect is its inducibility by various agents and/or treatments. In addition to NaF and ATP depletion [1, 4], propranolol [5–7], NaVO 3 [8], lead [10]or redox modification [9, 11]and, probably, also PGE2 [12]have been used as inducers. Despite the different molecular character of the individual inducers, their action involves the translocation of extracellular Ca 2+ across the RBC membrane which, finally, leads to the activation of K(Ca) and massive K + loss.…”