Effect of praeruptorin C on spontaneous [Ca2+]i transients in cultured myocardial cells of neonatal rats
Abstract
AIM: To study the effects of praeruptorin C (Pra-C) on [Ca2+]i transients in
cultured neonatal myocardiocytes.
METHOD: Using Ca(2+)-sensitive fluorescent indicator, Fura 2-AM, spontaneous
cytosolic Ca2+ transients were measured in cultured myocardial cells of neonatal
rats.
RESULTS: Pra-C 10, 30 mumol.L-1 caused a decrease in the peak of Ca2+ transients.
Pra-C 30 mumol.L-1 and 10-30 mumol.L-1 inhibited partly the stimulatory effects
of CaCl2 4.8 mmol.L-1 and Bay k 8644 100 nmol.L-1 on peak Ca2+ transients,
respectively. Pra-C did not cause any marked change in the basal [Ca2+]i level
between beats. Pra-C inhibited the reduced [Ca2+]i transients after inhibition of
sarcoplasmic reticulum Ca2+ release in ryanodine pretreated cells.
CONCLUSIONS: Pra-C inferred with the Ca2+ influx responsible for
excitation-contraction coupling in myocardiocytes.
Keywords:
cultured neonatal myocardiocytes.
METHOD: Using Ca(2+)-sensitive fluorescent indicator, Fura 2-AM, spontaneous
cytosolic Ca2+ transients were measured in cultured myocardial cells of neonatal
rats.
RESULTS: Pra-C 10, 30 mumol.L-1 caused a decrease in the peak of Ca2+ transients.
Pra-C 30 mumol.L-1 and 10-30 mumol.L-1 inhibited partly the stimulatory effects
of CaCl2 4.8 mmol.L-1 and Bay k 8644 100 nmol.L-1 on peak Ca2+ transients,
respectively. Pra-C did not cause any marked change in the basal [Ca2+]i level
between beats. Pra-C inhibited the reduced [Ca2+]i transients after inhibition of
sarcoplasmic reticulum Ca2+ release in ryanodine pretreated cells.
CONCLUSIONS: Pra-C inferred with the Ca2+ influx responsible for
excitation-contraction coupling in myocardiocytes.