Changes in intracellular Ca2+ concentration ([Ca2+](i)) induced by [Arg8]-vasopressin (AVP) were studied in cultured rat hippocampal neurons by fura-2 fluorometry. AVP (10-1,000 nM) caused a dose-dependent increase in [Ca2+](i). The selective V1 vasopressin receptor agonist [Phe2, Ile3, Orn8]vasopressin also induced a significant increase in [Ca2+](i), whereas the selective V2 vasopressin receptor agonist [deamino Cys1, D-Arg8]- vasopressin showed no effect. The AVP-induced increase in [Ca2+](i) was inhibited by the selective V1 vasopressin receptor antagonist d(CH2)5[Tyr2(Me), Arg8]-vasopressin and nonpeptide V1 antagonist OPC- 21268. On the other hand, no antagonistic effects were observed with the V2 vasopressin antagonist desglycinamide-[d(CH2)5, D-Ile2, Ile4, Arg8]- vasopressin and nonpeptide V2 antagonist OPC-31260. The increase in [Ca2+](i) induced by AVP was abolished after removal of extracellular Ca2+. In addition, AVP-induced [Ca2+](i) elevation was not affected by treatment with verapamil, which blocked the [Ca2+](i) increase induced by an isotonic high K+- medium (50 mM). However, ω-conotoxin GVIA completely inhibited the effect of AVP. These results suggested that the AVP-induced [Ca2+](i) increase in cultured rat hippocampal neurons is due to influx of Ca2+ through V1 VP receptors coupled with N-type calcium channels.
- Cultured rat hippocampal neuron
- V- Antagonist
- ω-Conotoxin GVIA
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