CAP(2b), a cardioacceleratory peptide, is present in Drosophila and stimulates tubule fluid secretion via cGMP

A cardioacceleratory peptide, CAP(2b), identified originally in the lepidopteran Manduca sexta, stimulates fluid secretion by Malpighian tubules of the dipteran Drosophila melanogaster. High-performance liquid chromatography analyses of adult D. melanogaster reveal the presence of a CAP(2b)-like peptide, that coelutes with M. sexta CAP(2b) and synthetic CAP(2b) and that has CAF(2b)-like effects on the M, sexta heart. CAP(2b), accelerates fluid secretion in tubules stimulated by adenosine 3',5'-cyclic monophosphate (cAMP) but has no effect on tubules stimulated by guanosine 3',5'-cyclic monophosphate (cGMP), implying that it acts through the latter pathway. By contrast, the action of leucokinin is additive to both cAMP and cGMP but not to thapsigargin, suggesting that leucokinin acts by the elevation of intracellular calcium. CAP(2b) stimulation elevates tubule cGMP levels but not those of cAMP. By contrast, leucokinin has no effect on levels of either cyclic nucleotide. Both CAP(2b), and cGMP increase transepithelial potential difference, suggesting that stimulation of vacuolar-adenosinetriphosphatase action underlies the corresponding increases in fluid secretion. Overall, the results show that a Drosophila CAP(2b)-related peptide acts to stimulate fluid secretion by Malpighian tubules through the cGMP-signaling pathway.