Article date: May 1994
By: Norimichi Nakahata, Hiromi Ishimoto, Kohichi Mizuno, Yasushi Ohizumi, Hironori Nakanishi, in Volume 112, Issue 1, pages 299-303
The effect of mastoparan, a wasp venom toxin, on intracellular free Ca2+ concentration ([Ca2+]i) was examined in human astrocytoma cells. Mastoparan inhibited [Ca2+]i induced by carbachol (100 μm) in a concentration‐dependent manner in the absence of extracellular Ca2+, consistent with our previous results showing that mastoparan inhibits phosphoinositide hydrolysis in human astrocytoma cells.
In contrast, mastoparan itself increased [Ca2+]i and augmented carbachol‐induced increase in the [Ca2+]i in the presence of extracellular Ca2+, suggesting that mastoparan elicited Ca2+ influx from the extracellular medium. The increase appeared to be maximum at extracellular Ca2+ concentrations of 0.1–0.2 mm. The higher concentrations of extracellular Ca2+ depressed the influx.
Pertussis toxin did not affect mastoparan‐induced inhibition of [Ca2+]i in the absence of extracellular Ca2+, consistent with the previous results that pertussis toxin did not affect mastoparan‐induced inhibition of phosphoinositide hydrolysis.
Pertussis toxin augmented mastoparan‐induced increase in [Ca2+]i in the presence of extracellular Ca2+, suggesting that pertussis toxin substrate(s) seems to be inhibitory for Ca2+ influx induced by mastoparan.
Verapamil, nifedipine and diltiazem (each 10 μm), L‐type Ca2+ antagonists, did not affect mastoparan‐induced Ca2+ influx. However, verapamil (10 μm) slightly inhibited the increase in [Ca2+]i induced by carbachol in the presence of mastoparan.
The results obtained in the present study indicate that mastoparan has two opposite effects on [Ca2+]i in human astrocytoma cells and possibly has at least two sites of action.
The effect of mastoparan, a wasp venom toxin, on intracellular free Ca2+ concentration ([Ca2+]i) was examined in human astrocytoma cells. Mastoparan inhibited [Ca2+]i induced by carbachol (100 μm) in a concentration‐dependent manner in the absence of extracellular Ca2+, consistent with our previous results showing that mastoparan inhibits phosphoinositide hydrolysis in human astrocytoma cells.
In contrast, mastoparan itself increased [Ca2+]i and augmented carbachol‐induced increase in the [Ca2+]i in the presence of extracellular Ca2+, suggesting that mastoparan elicited Ca2+ influx from the extracellular medium. The increase appeared to be maximum at extracellular Ca2+ concentrations of 0.1–0.2 mm. The higher concentrations of extracellular Ca2+ depressed the influx.
Pertussis toxin did not affect mastoparan‐induced inhibition of [Ca2+]i in the absence of extracellular Ca2+, consistent with the previous results that pertussis toxin did not affect mastoparan‐induced inhibition of phosphoinositide hydrolysis.
Pertussis toxin augmented mastoparan‐induced increase in [Ca2+]i in the presence of extracellular Ca2+, suggesting that pertussis toxin substrate(s) seems to be inhibitory for Ca2+ influx induced by mastoparan.
Verapamil, nifedipine and diltiazem (each 10 μm), L‐type Ca2+ antagonists, did not affect mastoparan‐induced Ca2+ influx. However, verapamil (10 μm) slightly inhibited the increase in [Ca2+]i induced by carbachol in the presence of mastoparan.
The results obtained in the present study indicate that mastoparan has two opposite effects on [Ca2+]i in human astrocytoma cells and possibly has at least two sites of action.
DOI: 10.1111/j.1476-5381.1994.tb13068.x
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