Disease relevance of capa

• By immunocytochemistry, we identified four pairs of neuroendocrine cells likely to release the capa peptides into the hemolymph: one pair in the subesophageal ganglion and the other three in the abdominal neuromeres [1].
• This manifests itself as hypersensitivity of epithelial fluid transport to the nitridergic neuropeptide, capa-1, which acts through nitric oxide and cGMP [2].

High impact information on capa

• Furthermore, a novel epithelial role is suggested for DG1, which is considerably more responsive to cGMP than to capa-1 stimulation [3].
• CAP2b-stimulated fluid transport and cytosolic calcium concentration ([Ca2+]i) increases are inhibited by the L-type calcium channel blockers verapamil and nifedipine. cGMP-stimulated fluid transport is verapamil and nifedipine sensitive [4].
• Amino acid sequence of CAP2b, an insect cardioacceleratory peptide from the tobacco hawkmoth Manduca sexta [5].
• Examination of several national computer protein data bases failed to reveal other peptides or proteins with any sequence homology to CAP2b indicating that this is likely to be a novel insect neuropeptide [5].
• The receptor was not activated by Drosophila neuropeptides, containing a C-terminal PRIamide sequence (such as ecdysis-triggering-hormone-2), or PRVamide (such as capa-1 and -2), or other neuropeptides and biogenic amines not related to the pyrokinins [6].

Anatomical context of capa

• Pyrokinin/PBAN-like peptides in the central nervous system of Drosophila melanogaster [7].
• Overall, the results show that a Drosophila CAP2b-related peptide acts to stimulate fluid secretion by Malpighian tubules through the cGMP-signaling pathway [8].
• The neuropeptide cardioacceleratory peptide 2b (CAP2b) has been previously shown to stimulate fluid secretion in this epithelium by elevating intracellular cGMP levels [9].

Associations of capa with chemical compounds

• In D. melanogaster Malpighian (renal) tubules, the capa peptides stimulate production of nitric oxide (NO) and guanosine 3', 5'-cyclic monophosphate (cGMP), resulting in increased fluid transport [10].
• By contrast, either cyclic AMP or cyclic GMP (upon CAP2b stimulation) acts on the electrogenic cation-transporting apical V-ATPase, with only a negligible effect on anion conductance and without perturbing intracellular [Ca2+] [11].
• The cell-permeant Ca2+ chelator BAPTA-AM was shown to suppress the action of leucokinins (insect peptides that induce rapid fluid secretion), but not those of cyclic AMP, the neuronally derived insect peptide cardioacceleratory peptide 2b (CAP2b) or its intracellular messenger cyclic GMP [11].
• These data indicate that CAP2b stimulates NOS and therefore, endogenous NO production, which, in turn, stimulates a soluble guanylate cyclase [9].

Other interactions of capa

• Because capa-1 and -2 and related insect neuropeptides stimulate fluid secretion in insect Malpighian (renal) tubules, the identification of this first insect capa receptor will advance our knowledge on insect renal function [12].
• In situ tissue hybridization further suggests FLT is a novel brain-gut peptide and specifically, the measured activity indicates that it is a potent myotropin [13].
• Therefore, it was of interest to investigate if CAP2b acts through NO in isolated tubules and thus presumably through stimulation of a tubule NO synthase (NOS) [9].

Analytical, diagnostic and therapeutic context of capa

• Molecular cloning and functional expression of a Drosophila receptor for the neuropeptides capa-1 and -2 [12].
• The primary structure of a novel insect neuropeptide, Cardioacceleratory Peptide 2b (CAP2b), from the tobacco hawkmoth Manduca sexta has been established using a combination of mass spectroscopy, Edman degradation microsequencing, amino acid analysis, and biological assays [5].

References