Effects of bipyridylium compounds on calcium release from triadic vesicles isolated from rabbit skeletal muscle

Abstract

1 The effects of l,l'-diheptyl-4,4'-bipyridinium dibromide (DHBP), a viologen for electrochromic memory display agent, on calcium release and ryanodine binding were studied with triad-rich sarcoplasmic reticulum (SR} vesicles isolated from rabbit skeletal muscle.2 DHBP inhibited the calcium release induced by 2 mM caffeine and 2 gg ml-I polylysine with an IC50 value of 5 gg ml1 and 4 pg ml1 respectively. 4 Calcium uptake by SR was inhibited in the presence of caffeine and this inhibition was antagonized by concomitant addition of DHBP. 5 The effect of DHBP on muscle twitches was studied on the mouse diaphragm. Muscle twitches elicited by direct electrical muscle stimulation and contractions induced by either 10 mM caffeine or 1 fLM ryanodine were blocked by pretreatment with DHBP. 6 Data from this study provided evidence that DHBP blocked the calcium release from SR by direct interaction with the calcium release channel, also known as the ryanodine receptor. A possible use of this agent as a specific inhibitor for calcium release and as a muscle relaxant was suggested.

Permissive role of calcium on regulatory volume decrease in freshly isolated mouse cholangiocytes

“…5a, the RVD of BDCCs treated with ryanodine at 200 nM (n=9) or 10 μM (n=7) was not different from that of the untreated controls (n=10). To further confirm this finding, the effect of dihydropyridine dibromide (DHBP), an inhibitor of calcium release from the endoplasmic reticulum [22], on RVD was examined as shown in Fig. 5b.…”

A Direct Mass-action Mechanism Explains Capacitative Calcium Entry in Jurkat and Skeletal L6 Muscle Cells

“…DHBP, another blocker of the RyR (25,26), was able to inhibit the Tg-induced rise in cytosolic Ca 2ϩ (Fig. 2).…”

Bidirectional Regulation of Ca2+/Calmodulin-Dependent Protein Kinase II Activity by Dopamine D4Receptors in Prefrontal Cortex

“…5, A and B, application of 2APB (30 M), a membrane-permeable IP 3 R antagonist (Hamada et al, 1999), abolished the D 4 effect on CaMKII activation (0.9 Ϯ 0.2-fold, n ϭ 10). In contrast, DHBP (30 g/ml), a potent RyR antagonist (Kang et al, 1994), failed to alter the D 4 enhancement of CaMKII activity (3.6 Ϯ 0.9-fold, n ϭ 6). Pretreatment of PFC slices with the intracellular calcium pump inhibitor thapsigargin (5 M, 30 min) to deplete internal stores of Ca 2ϩ also eliminated the D 4 effect on CaMKII activation (1.0 Ϯ 0.2-fold, n ϭ 8).…”