CAP2b, a cardioacceleratory peptide, is present in Drosophila and stimulates tubule fluid secretion via cGMP

1995 ◽  
Vol 269 (6) ◽  
pp. R1321-R1326 ◽  
Author(s):  
S. A. Davies ◽  
G. R. Huesmann ◽  
S. H. Maddrell ◽  
M. J. O'Donnell ◽  
N. J. Skaer ◽  
...  

A cardioacceleratory peptide, CAP2b, 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 CAP2b-like peptide, that coelutes with M. sexta CAP2b and synthetic CAP2b and that has CAP2b-like effects on the M. sexta heart. CAP2b 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. CAP2b stimulation elevates tubule cGMP levels but not those of cAMP. By contrast, leucokinin has no effect on levels of either cyclic nucleotide. Both CAP2b 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 CAP2b-related peptide acts to stimulate fluid secretion by Malpighian tubules through the cGMP-signaling pathway.

1993 ◽  
Vol 178 (1) ◽  
pp. 231-243 ◽  
Author(s):  
N. Audsley ◽  
G. M. Coast ◽  
D. A. Schooley

1. Manduca sexta diuretic hormone (Mas-DH) stimulates fluid secretion by adult Malpighian tubules of M. sexta, demonstrating its site of diuretic action in M. sexta for the first time. It was not possible to develop a suitable bioassay to measure fluid secretion in larval proximal tubules. 2. Mas-DH has an antidiuretic action on the cryptonephric complex of larval M. sexta because it increases fluid absorption from the rectum. It appears that in this complex Mas-DH is acting on a Na+/K+/2Cl- co-transporter, presumably on the basal membrane of the cryptonephric Malpighian tubules, because Mas-DH-stimulated fluid absorption by the cryptonephric complex is inhibited by bumetanide or the removal of Cl-, Na+ or K+ from the haemolymph side of the tissue. This is the first demonstration of hormonal control of fluid absorption by the cryptonephric complex. 3. Concomitant with the stimulation of fluid transport, Mas-DH increases the amount of cyclic AMP secreted by adult Malpighian tubules and the cryptonephric complex. In addition, Mas-DH promotes cyclic AMP production by the larval proximal tubules.


1997 ◽  
Vol 200 (17) ◽  
pp. 2363-2367 ◽  
Author(s):  
M C Quinlan ◽  
N J Tublitz ◽  
M J O'Donnell

Rhodnius prolixus eliminates NaCl-rich urine at high rates following its infrequent but massive blood meals. This diuresis involves stimulation of Malpighian tubule fluid secretion by diuretic hormones released in response to distention of the abdomen during feeding. The precipitous decline in urine flow that occurs several hours after feeding has been thought until now to result from a decline in diuretic hormone release. We suggest here that insect cardioacceleratory peptide 2b (CAP2b) and cyclic GMP are part of a novel mechanism of anti-diuresis. Secretion rates of 5-hydroxytryptamine-stimulated Malpighian tubules are reduced by low doses of CAP2b or cyclic GMP. Maximal secretion rates are restored by exposing tubules to 1 mmol l-1 cyclic AMP. Levels of cyclic GMP in isolated tubules increase in response to CAP2b, consistent with a role for cyclic GMP as an intracellular second messenger. Levels of cyclic GMP in tubules also increase as urine output rates decline in vivo, suggesting a physiological role for this nucleotide in the termination of diuresis.


1994 ◽  
Vol 267 (1) ◽  
pp. C236-C244 ◽  
Author(s):  
J. Geiger ◽  
C. Nolte ◽  
U. Walter

Stimulation of Ca2+ mobilization and entry by agonists such as ADP, thrombin, and thromboxane is an early step of platelet activation. Here, we compared the effects of adenosine 3',5'-cyclic monophosphate (cAMP)-elevating prostaglandins, guanosine 3',5'-cyclic monophosphate (cGMP)-elevating nitrovasodilators, membrane-permeant selective activators of cAMP- or cGMP-dependent protein kinases, and physiological endothelium-derived factors on the agonist-evoked Ca2+ mobilization and entry in human platelets. Prostaglandin E1, the prostacyclin analogue Iloprost, the nitric oxide (NO) donor 3-morpholinosydnonimine hydrochloride, and selective activators of cGMP- or cAMP-dependent protein kinase strongly inhibited the agonist-evoked Ca2+ mobilization from intracellular stores and associated late Ca2+ entry but had little effects on the rapid (1st) phase of ADP-evoked Ca2+ entry. During coincubation of platelets with endothelial cells, endothelium-derived factors that were released strongly inhibited platelet agonist-evoked Ca2+ mobilization and only moderately affected the rapid phase of ADP-evoked Ca2+ entry. These effects were partially prevented when endothelial cells were preincubated with cyclooxygenase and/or NO synthase inhibitors. Endothelial cells therefore produce sufficient quantities of labile platelet inhibitors whose effects on the platelet Ca2+ response resemble those observed with selective cAMP- and cGMP-dependent protein kinase activators.


2005 ◽  
Vol 289 (3) ◽  
pp. C708-C716 ◽  
Author(s):  
Franca Golin-Bisello ◽  
Neil Bradbury ◽  
Nadia Ameen

The cystic fibrosis transmembrane conductance regulator (CFTR) is critical to cAMP- and cGMP-activated intestinal anion secretion and the pathogenesis of secretory diarrhea. Enterotoxins released by Vibrio cholerae (cholera toxin) and Escherichia coli (heat stable enterotoxin, or STa) activate intracellular cAMP and cGMP and signal CFTR on the apical plasma membrane of small intestinal enterocytes to elicit chloride and fluid secretion. cAMP activates PKA, whereas cGMP signals a cGMP-dependent protein kinase (cGKII) to phosphorylate CFTR in the intestine. In the jejunum, cAMP also regulates CFTR and fluid secretion by insertion of CFTR from subapical vesicles to the surface of enterocytes. It is unknown whether cGMP signaling or phosphorylation regulates the insertion of CFTR associated vesicles from the cytoplasm to the surface of enterocytes. We used STa, cell-permeant cGMP, and cAMP agonists in conjunction with PKG and PKA inhibitors, respectively, in rat jejunum to examine whether 1) cGMP and cGK II regulate the translocation of CFTR to the apical membrane and its relevance to fluid secretion, and 2) PKA regulates cAMP-dependent translocation of CFTR because this intestinal segment is a primary target for toxigenic diarrhea. STa and cGMP induced a greater than fourfold increase in surface CFTR in enterocytes in association with fluid secretion that was inhibited by PKG inhibitors. cAMP agonists induced a translocation of CFTR to the cell surface of enterocytes that was prevented by PKA inhibitors. We conclude that cAMP and cGMP-dependent phosphorylation regulates fluid secretion and CFTR trafficking to the surface of enterocytes in rat jejunum.


1997 ◽  
Vol 25 (01) ◽  
pp. 37-50 ◽  
Author(s):  
Koji Miyamoto ◽  
Takeshi Katsuragi ◽  
Parhat Abdu ◽  
Tatsuo Furukawa

Effects of baicalein on release of slow reacting substance of anaphylaxis (SRS-A) or leukotriene (L T) from the sensitized guinea pig lung after antigen challenge and tonus of guinea pig tracheal muscles were studied. Baicalein inhibited release of SRS-A from sensitized guinea pig lung after antigen challenge. High-performance liquid chromatography (HPLC) analysis revealed that released SRS-A consisted of LTC 4 and D 4. Baicalein also reduced release of LTC 4 and D 4 from the sensitized lung after antigen challenge. Baicalein relaxed the isolated guinea pig tracheal smooth muscle contracted by LTD 4, carbachol or histamine. However, this compound produced a contraction when the tracheal muscle was contracted by prostaglandin F 2α ( PGF 2α). This contraction by baicalein was abolished by pretreatment with indomethacin, a cyclooxygenase inhibitor. Baicalein elicited a relaxation in the normal non-sensitized tracheal preparation but a contraction in the tissue isolated from actively sensitized guinea pig in 4 among 7 cases. Baicalein also produced a contraction in the trachea pretreated with phorbol dibutyrate and contracted by carbachol, which was eliminated after treatment with indomethacin. The results suggest that baicalein exerts action via, at least, two different mechanisms, the inhibition of releasing SRS-A (LTs) and direct relaxing effects on the trachea. Besides, baicalein seems to produce contraction under certain conditions, which may involve stimulation of the cyclooxygenase pathway.


1997 ◽  
Vol 200 (1) ◽  
pp. 117-127 ◽  
Author(s):  
S Adamo ◽  
C Linn ◽  
N Beckage

The parasitoid wasp Cotesia congregata lays its eggs within the body of its host, the larval form of the tobacco hornworm Manduca sexta. Host behaviour appeared normal until approximately 8 h prior to the emergence of the parasitoids from their host at which time M. sexta feeding and locomotion declined irreversibly. This change in host behaviour may be to the advantage of the wasp since unparasitized M. sexta presented with wasp pupae ate them. Despite the decline in feeding and locomotion, hosts with emerged parasitoids had normal reflexes and showed no other signs of debilitation. Concomitant with the change in host behaviour, octopamine concentration measured using high-performance liquid chromatography with electrochemical detection (HPLC-ED) increased from 22.2±2.1 pg µl-1 to 143.7±7.8 pg µl-1 in the haemolymph of the host. In unparasitized M. sexta, however, increased octopamine levels were correlated with increased activity. We discuss possible explanations for the co-occurrence of high haemolymph octopamine levels and low behavioural arousal in parasitized M. sexta.


1993 ◽  
Vol 177 (1) ◽  
pp. 273-285 ◽  
Author(s):  
S. H. Maddrell ◽  
M. J. O'Donnell ◽  
R. Caffrey

The blood-sucking insect Rhodnius prolixus rapidly eliminates a Na(+)-rich K(+)-poor urine after its large meals. K(+)-rich fluid is first secreted by the upper Malpighian tubules and passes to the lower tubules where most of the potassium is reabsorbed. During the initial stimulation of the tubules, the lower tubules must be activated first to avoid loss of potassium. The major element in this is that they respond more rapidly than do the upper tubules to particular hormonal concentrations rather than that they react to lower hormonal concentrations than do the upper tubules. During subsequent diuresis, regulation of the haemolymph potassium concentration depends on three cooperative homoeostatic mechanisms in the tubules. A fall in potassium concentration of the medium bathing the tubules causes (i) a decrease in the rate of fluid secretion by the upper tubules, (ii) a decrease in potassium concentration in the fluid secreted by the upper tubules and (iii) an increase in the rate of potassium absorption by the lower tubules. The tubules respond in the opposite direction to an increase in potassium concentration of the medium. As a result, the potassium concentration of the urine can be adjusted to match the potassium concentration of the fluids absorbed from the gut, so that the potassium concentration of the insect's haemolymph remains unaltered.


1980 ◽  
Vol 58 (3) ◽  
pp. 243-248 ◽  
Author(s):  
N. Schlageter ◽  
R. A. Janis ◽  
R. T. Gualtieri ◽  
O. Hechter

The effects of oxytocin and methacholine on cyclic nucleotide levels in estrogen-primed rabbit myometrium were studied in the presence and absence of 1-methyl-3-isobutyl xanthine (MIX), a phosphodiesterase inhibitor. In the absence of MIX, methacholine increased guanosine 3′,5′-cyclic monophosphate (cGMP) levels at a time when contraction was decreasing, but had no influence on adenosine 3′,5′-cyclic monophosphate (cAMP) levels. In contrast, oxytocin did not elevate cGMP, but rapidly increased cAMP levels. MIX (1 mM) increased both cAMP and cGMP levels. Oxytocin or methacholine further increased cGMP, indicating activation of guanylate cyclase. Oxytocin- but not methacholine-induced stimulation of guanylate cyclase was abolished in Ca2+-free solution. Oxytocin increased cAMP over the levels produced by MIX alone, whereas methacholine decreased cAMP below the MIX control values; these effects were insensitive to indomethacin. Tissue levels of cGMP and cAMP did not directly correlate with isometric tension. The results also indicate that both oxytocin and methacholine stimulate guanylate cyclase but have opposing effects on adenylate cyclase of rabbit myometrium.


1989 ◽  
Vol 67 (6) ◽  
pp. 1495-1499 ◽  
Author(s):  
R. J. Martin ◽  
R. G. H. Downer

The capacity of several tissues of the American cockroach, Periplaneta americana, to remove p-octopamine from incubation medium was investigated using high performance liquid chromatography with electrochemical detection to monitor levels of p-octopamine and the N-acetylated derivative. Gut was the most active tissue in removing p-octopamine from the medium and separate analyses of the various regions of the gut indicate that the Malpighian tubules constitute the primary site of removal. Epidermal and nervous tissue are also capable of removing substantial amounts of p-octopamine. In addition to the removal of p-octopamine, Malpighian tubules remove dopamine and 5-hydroxytryptamine from incubation medium and, indeed, have a slightly greater capacity for removing these monoamines than for removing p-octopamine. However, concentrations of each amine that are considerably in excess of physiological levels do not saturate the system. Most of the p-octopamine removed by the gut tissue undergoes N-acetylation to form N-acetyl-p-octopamine; thus, this appears to be the primary degradation metabolic route for p-octopamine. Analysis of the faeces following injection of p-octopamine demonstrated the presence of both p-octopamine and the N-acetylated derivative.


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