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First published online November 2, 2007
Journal of Experimental Biology 210, 3979-3989 (2007)
Published by The Company of Biologists 2007
doi: 10.1242/jeb.006056

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An antidiuretic peptide (Tenmo-ADFb) with kinin-like diuretic activity on Malpighian tubules of the house cricket, Acheta domesticus (L.)

Geoffrey M. Coast^1,*, Ronald J. Nachman² and David A. Schooley³

¹ School of Biological and Chemical Sciences, Birkbeck, University of London, Malet Street, London WC1E 7HX, UK
² US Department of Agriculture, APMRU/SPARC, College Station, TX 77845, USA
³ Biochemistry, University of Nevada, Reno, NV 89557, USA

^* Author for correspondence (e-mail: g.coast{at}bbk.ac.uk)

Accepted 3 September 2007

Acheta domesticus is reported to have an antidiuretic hormone that reduces Malpighian tubule secretion. Identified peptides known to work in this way (Tenmo-ADFa and ADFb, and Manse-CAP_2b) were tested as candidates for the unidentified hormone, along with their second messenger, cyclic GMP. Only Tenmo-ADFb was active, but was diuretic, as was 8-bromo cyclic GMP. The activity of Tenmo-ADFb is comparable to that of the cricket kinin neuropeptide, Achdo-KII, but it is much less potent. Its activity was unaffected by deleting either the six N-terminal residues or the C-terminal phenylalanine.

At high concentrations, tubule secretion is doubled by Tenmo-ADFb and Achdo-KII, but their actions are non-additive, suggesting they have a similar mode of action. Both stimulate a non-selective KCl and NaCl diuresis, which is consistent with the opening of a transepithelial Cl^– conductance. In support of this, the diuretic response to Tenmo-ADFb and Achdo-KII is prevented by a ten-fold reduction in bathing fluid chloride concentration, and both peptides cause the lumen-positive transepithelial voltage to collapse. The Cl^– conductance pathway appears likely to be transcellular, because the Cl^– channel blocker DPC reduces both basal and peptide-stimulated rates of secretion. The effects of 8-bromo cyclic GMP on transepithelial voltage and composition of the secreted fluid are markedly different from those of Tenmo-ADFb.

This is the first report of the antidiuretic factor Tenmo-ADFb stimulating tubule secretion. Although the actions of Tenmo-ADFb are indistinguishable from those of Achdo-KII, it is unlikely to act at a kinin receptor, because the core sequence (residues 7–12) lacks the Phe and Trp residues that are critical for kinin activity.

Key words: Malpighian tubule, fluid secretion, ion transport, electrophysiology, diuretic hormone, antidiuretic factor, kinin neuropeptide

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