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  • Title: Arginine vasopressin increases intracellular calcium ion concentration in isolated mouse collecting tubule cells: distinct mechanism of action through V2 receptor, but independent of adenylate cyclase activation.
    Author: Naruse M.
    Journal: Nihon Jinzo Gakkai Shi; 1992 Apr; 34(4):337-47. PubMed ID: 1635278.
    Abstract:
    The effects of arginine vasopressin (AVP*2) and its V2 receptor agonist, 1-deamino-8-D-AVP (dDAVP), on the intracellular calcium ion concentration ([Ca2+]i) in isolated collecting tubular cells of mouse kidney were examined using fluorescent indicator fura-2 and a superfusion system. Both AVP and dDAVP evoked a rapid, transient increase followed by a sustained elevation of [Ca2+]i in CCT, OMCT, and IMCT in a dose-dependent manner. In CCT, the increments in [Ca2+]i by dDAVP were lower than those induced by AVP at all concentrations (10(-10)-10(-6) M) of the agonists tested, while in OMCT and IMCT, the increments were comparable. The initial peak of the rise in [Ca2+]i induced by AVP and dDAVP in these collecting tubule segments was partially attenuated by about 40% and the second sustained elevation was largely abolished in the absence of Ca2+ in the superfusate. Further, the increments [Ca2+]i induced by AVP were not affected by the addition of nicardipine to the superfusate. The increases in [Ca2+]i evoked by AVP and dDAVP were not mimicked by cAMP or forskolin. Moreover, they were not affected by alpha-adrenergic stimulation with epinephrine, in the presence and absence of prazosin, conditions which inhibit AVP-dependent cAMP production. These results indicate that AVP increases [Ca2+]i in CCT, OMCT, and IMCT, probably through V2 receptors, but via a mechanism which is independent of adenylate cyclase activation. In addition, the rise in [Ca2+]i is due to both Ca2+ release from the intracellular stores and increased Ca2+ influx through Ca2+ channels insensitive to nicardipine.
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