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Am J Physiol Renal Physiol 283: F499-F508, 2002. First published April 10, 2002; doi:10.1152/ajprenal.00041.2002
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Vol. 283, Issue 3, F499-F508, September 2002

Leucokinin activates Ca2+-dependent signal pathway in principal cells of Aedes aegypti Malpighian tubules

Ming-Jiun Yu and Klaus W. Beyenbach

Department of Biomedical Sciences, Cornell University, Ithaca, New York 14853

The role of Ca2+ in mediating the diuretic effects of leucokinin-VIII was studied in isolated perfused Malpighian tubules of the yellow fever mosquito, Aedes aegypti. Peritubular leucokinin-VIII (1 µM) decreased the transepithelial resistance from 11.2 to 2.6 kOmega · cm, lowered the transepithelial voltage from 42.8 to 2.7 mV, and increased transepithelial Cl- diffusion potentials 5.1-fold. In principal cells of the tubules, leucokinin-VIII decreased the fractional resistance of the basolateral membrane from 0.733 to 0.518. These effects were reversed by the peritubular Ca2+-channel blocker nifedipine, suggesting a role of peritubular Ca2+ and basolateral Ca2+ channels in signal transduction. In Ca2+-free Ringer bath, the effects of leucokinin-VIII were partial and transient but were fully restored after the bath Ca2+ concentration was restored. Increasing intracellular Ca2+ with thapsigargin duplicated the effects of leucokinin-VIII, provided that peritubular Ca2+ was present. The kinetics of the effects of leucokinin-VIII is faster than that of thapsigargin, suggesting the activation of inositol-1,4,5-trisphosphate-receptor channels of intracellular stores. Store depletion may then bring about Ca2+ entry into principal cells via nifedipine-sensitive Ca2+ channels in the basolateral membrane.

nifedipine; thapsigargin


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