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PubMed1999

[Role of chlorine transporters and water channels in autosomal dominant polycystic kidneys].

The molecular identification of several transporters has allowed a better understanding of the mechanism involved in cyst fluid accumulation in the autosomal dominant polycystic kidney disease (ADPKD). This fluid secretion is mediated by Cl- secretion, the latter process being stimulated by cyclic AMP. At the cellular level, Cl- secretion is carried out by a basolateral, bumetanide-sensitive cotransporter, organized in series with an apical CFTR channel. The accumulation of Cl- in the cyst lumen attracts Na+ (electric coupling) and water (osmotic coupling), the movement of the latter being partially mediated by aquaporins. The understanding of cyst fluid secretion mechanisms will be helpful to elaborate new therapeutic strategies aiming at slowing cyst expansion and preserving renal function.

Aquaporins↗
PubMed1983

Differentiation of secretagogue drugs by chlorpromazine in rat intestine in vivo.

The effect of chlorpromazine (CPZ) on passive epithelial permeability and net fluid movement induced by secretagogues was tested in the rat intestine in vivo. CPZ, in a dose of 20 mg/kg intramuscularly, did not alter colonic permeability either in control conditions or during increased permeability caused by deoxycholic acid (DOC) or bisacodyl. Fluid secretion induced by cholera toxin and theophylline was strongly reduced by CPZ. The effects of oxyphenisatin and bisacodyl were only slightly but significantly inhibited by CPZ, whereas the action of DOC was unaffected. It is concluded, that the increase of the epithelial permeability is the main reason for the augmented fluid secretion caused by DOC. Bisacodyl and oxyphenisatin seem to act partly via an increase in permeability and to some degree via an induction of an active secretory process.

Animals↗
PubMed1975

The innervation of the salivary gland of the moth, Manduca sexta: evidence that dopamine is the transmitter.

1. Using the Falck-Hillarp histochemical technique for monoamines, evidence was found for the presence of a catecholamine in the salivary gland nerves of the moth, Manduca sexta. 2. The innervation was studied with the electron microscope. Only the fluid-secreting region of the gland is innervated and the nerve endings are characteristic of monoamine-containing terminals. 3. Using a sensitive enzymatic-isotopic assay for catecholamines, it was found that whole salivary glands contain 0.33 mug/g dopamine but no noradrenaline. 4. It seems likely that dopamine mediates fluid-secretion in the salivary gland of Manduca as it does a number of other arthropods.

Animals↗
PubMed2005

Transfer of the AQP1 cDNA for the correction of radiation-induced salivary hypofunction.

The treatment of most patients with head and neck cancer includes ionizing radiation (IR). Salivary glands in the IR field suffer significant and irreversible damage, leading to considerable morbidity. Previously, we reported that adenoviral (Ad)-mediated transfer of the human aquaporin-1 (hAQP1) cDNA to rat [C. Delporte, B.C. O'Connell, X. He, H.E. Lancaster, A.C. O'Connell, P. Agre, B.J. Baum, Increased fluid secretion after adenoviral-mediated transfer of the aquaporin-1 cDNA to irradiated rat salivary glands. Proc. Natl. Acad. Sci. U S A. 94 (1997) 3268-3273] and miniature pig [Z. Shan, J. Li, C. Zheng, X. Liu, Z. Fan, C. Zhang, C.M. Goldsmith, R.B. Wellner, B.J Baum, S. Wang. Increased fluid secretion after adenoviral-mediated transfer of the human aquaporin-1 cDNA to irradiated miniature pig parotid glands. Mol. Ther. 11 (2005) 444-451] salivary glands approximately 16 weeks following IR resulted in a dose-dependent increase in salivary flow to > or =80% control levels on day 3. A control Ad vector was without any significant effect on salivary flow. Additionally, after administration of Ad vectors to salivary glands, no significant lasting effects were observed in multiple measured clinical chemistry and hematology values. Taken together, the findings show that localized delivery of AdhAQP1 to IR-damaged salivary glands is useful in transiently increasing salivary secretion in both small and large animal models, without significant general adverse events. Based on these results, we are developing a clinical trial to test if the hAQP1 cDNA transfer strategy will be clinically effective in restoring salivary flow in patients with IR-induced parotid hypofunction.

Animals↗
PubMed1990

The role of prostanoids in the production of acute acalculous cholecystitis by platelet-activating factor.

Gallbladder tissue from patients with acute acalculous cholecystitis contains increased amounts of prostanoids when compared to normal gallbladder tissue. Platelet-activating factor (PAF) is a potent stimulus of eicosanoid formation. It has been implicated as a mediator of acute inflammatory processes and systemic responses to shock. In this study the role of PAF in acute acalculous cholecystitis was evaluated. Anesthetized cats underwent gallbladder perfusion with a physiologic buffer solution containing [14C]polyethylene glycol as a nonabsorbable tracer to quantitate mucosal water absorption. Platelet-activating factor was infused into the hepatic artery for 2 hours. Control experiments were performed when vehicle alone was infused. Experiments also were performed when indomethacin was administered intravenously and when indomethacin and PAF were administered. Gallbladder mucosal absorption/secretion and perfusate and tissue prostaglandin E (PGE) and 6 keto prostaglandin F1 alpha (6-keto PGF1 alpha) levels were evaluated. Gallbladder inflammation was evaluated by beta-glucuronidase and myeloperoxidase tissue concentrations and by a histologic scoring system. Platelet-activating factor eliminated gallbladder absorption and produced net fluid secretion associated with dose-related increases in perfusate PGE concentrations and gallbladder tissue PGE and 6 keto PGF1 alpha levels when compared to control values. Platelet-activating factor produced significant inflammation in the gallbladder with increases in the histologic score of inflammation and tissue lysosomal enzyme activities. Indomethacin significantly decreased the fluid secretion, prostanoid levels, and inflammation produced by PAF. The results suggest that PAF may induce acute gallbladder inflammation associated with systemic stress through a prostanoid-mediated mechanism.

6-Ketoprostaglandin F1 alpha↗
PubMed2003

cAMP-dependent exocytosis and vesicle traffic regulate CFTR and fluid transport in rat jejunum in vivo.

The cystic fibrosis transmembrane conductance regulator (CFTR) channel is regulated by cAMP-dependent vesicle traffic and exocytosis to the apical membrane in some cell types, but this has not been demonstrated in the intestinal crypt. The distribution of CFTR, lactase (control), and fluid secretion were determined in rat jejunum after cAMP activation in the presence of nocodazole and primaquine to disrupt vesicle traffic. CFTR and lactase were localized by immunofluorescence, and surface proteins were detected by biotinylation of enterocytes. Immunoprecipitates from biotinylated and nonbiotinylated cells were analyzed by streptavidin detection and immunoblots. Immunolocalization confirmed a cAMP-dependent shift of CFTR but not lactase from a subapical compartment to the apical surface associated with fluid secretion that was reduced in the presence of primaquine and nocodazole. Analysis of immunoblots from immunoprecipitates after biotinylation revealed a 3.8 +/- 1.7-fold (P < 0.005) increase of surface-exposed CFTR after vasoactive intestinal peptide (VIP). These measurements provide independent corroboration supporting a role for vesicle traffic in regulating CFTR and cAMP-induced fluid transport in the intestine.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1997

Comparison of effects of uroguanylin, guanylin, and Escherichia coli heat-stable enterotoxin STa in mouse intestine and kidney: evidence that uroguanylin is an intestinal natriuretic hormone.

BACKGROUND: Uroguanylin and guanylin are intestinal peptides that activate a receptor-guanylate cyclase, which is also a receptor for Escherichia coli heat-stable enterotoxin (STa). These peptides may have a role in the body's regulation of fluid and electrolytes. METHODS: STa, bioactive guanylin, and bioactive uroguanylin were evaluated for effects in: 1) the suckling mouse intestinal fluid secretion assay; 2) an in vitro suckling mouse intestinal loop assay; 3) an intestinal receptor autoradiography assay; 4) a control or agonist-stimulated assay for cGMP response in T84 cells; and 5) an in vivo renal function assay in mice. RESULTS: In vivo, orally administered uroguanylin and STa but not guanylin, stimulated intestinal fluid secretion. All three peptides activated intestinal guanylate cyclase and had common intestinal receptors. In vitro, after pretreatment with chymotrypsin, only uroguanylin and STa retained agoinst activity. Chymostatin preserved guanylin activity. STa and uroguanylin induced diuresis, natriuresis, and kaliuresis. Guanylin was less potent than uroguanylin and STa. CONCLUSIONS: The results suggest that the endogenous intestinal peptides, uroguanylin and guanylin, regulate water and electrolyte homeostasis both through local effects on intestinal epithelia and endocrine effects on the kidney.

Animals↗
PubMed1979

Transepithelial permeability in the rabbit pancreas.

1. The transepithelial permeability in the isolated rabbit pancreas has been studied with the aid of radioactive markers added to the bathing medium. 2. After addition of these compounds in 2 mM concentration to the medium, they equilibrate within 30 min to a steady-state concentration in the secreted fluid. The latter concentrations, expressed as percent of those in the bathing medium, are: urea 100%, glycerol 90%, erythritol 95%, mannitol 60%, lactose 5%, sucrose 4% and inulin 3%. 3. Addition of 10(-5) M carbachol to the bathing medium after 60 or 90 min of incubation results in an increase of the concentrations of mannitol, lactose sucrose and inulin in the secreted fluid. Maximal concentrations, reached about 35 min after addition of the stimulant, are: mannitol 65%, lactose 31%, sucrose 23%, inulin 8%. 4. No change in the concentration of urea is observed, while the concentrations of glycerol and erythritol increase always to 100% after addition of 10(-5) M carbachol. 5. For sucrose and lactose the increase in permeability appears to be dependent on the concentration of carbachol. 6. There is no increase in the extracellular space for lactose, sucrose and inulin after incubating fragments of the rabbit pancreas with 10(-5) M carbachol. 7. Addition of atropine 5 min or more after carbachol stimulation has no effect on enzyme secretion, but markedly inhibits the increase in sucrose permeability. 8. These results indicate that: (a) the permeability of the transcellular transport route in the isolated rabbit pancreas is determined by the size of the permeating molecules, (b) this route is probably extracellular, (c) its permeability is increased by a cholinergic agent in dose-dependent fashion, (d) the increase in permeability is not caused by the enzyme secretion as such.

Animals↗
PubMed1997

Analysis of epithelial transport by measurement of K+, Cl- and pH gradients in extracellular unstirred layers: ion secretion and reabsorption by Malpighian tubules of Rhodnius prolixus

Summary The pH and concentrations of K+ and Cl- in the unstirred layer (USL) associated with the basolateral surfaces of the upper and lower Malpighian tubules of Rhodnius prolixus were measured using extracellular ion-selective microelectrodes. When stimulated with 5-hydroxytryptamine (5-HT) in vitro, the upper Malpighian tubule secretes Na+, K+, Cl- and water at high rates; the lower Malpighian tubule reabsorbs K+ and Cl- but not water. Concentrations of K+ and Cl- in the unstirred layer of the lower Malpighian tubule ([K+]USL, [Cl-]USL) were greater than those in the bathing saline, consistent with the accumulation of K+ and Cl- in the USL during 5-HT-stimulated KCl reabsorption. [K+]USL exceeded [K+]Bath by as much as 5.3-fold. Calculations of K+ flux based on measurements of [K+]USL at various distances from the tubule surface agreed well with flux calculated from the rate of fluid secretion and the change in K+ concentration of the secreted fluid during passage through the lower tubule. Concentrations of K+ in the unstirred layer of the upper Malpighian tubule were reduced relative to those in the bathing saline, consistent with depletion of K+ from the USL during 5-HT-stimulated secretion of K+ from bath to lumen. Changes in [K+]USL during 5-HT-stimulated K+ secretion from single upper Malpighian tubule cells could be resolved. Although differences between [K+]USL and [K+]Bath were apparent for upper and lower tubules in an in situ preparation, they were reduced relative to the differences measured using isolated tubules. We suggest that convective mixing of the fluids around the tubules by contractions of the midgut and hindgut reduces, but does not eliminate, differences between [K+]USL and [K+]Bath in situ. The USL was slightly acidic relative to the bath in 5-HT-stimulated upper and lower tubules; contributions to USL acidification are discussed. The results also show that the techniques described in this paper can resolve rapid and localized changes in ion transport across different regions of Malpighian tubules in response to stimulants or inhibitors of specific membrane transporters.

Journal Article↗
PubMed1986

Effect of atropine on pancreatic secretion in conscious rats.

The effect of atropine on exocrine pancreatic secretion was investigated in conscious rats. Intravenous atropine infusion decreased nonstimulated protein secretion during recirculation of pancreatic juice into the duodenum D50 = 15-20 micrograms/kg/h. The maximum inhibition from protein secretion (-89%) was obtained with 600 micrograms/kg/h. With larger doses, the inhibition was less. The response to secretin and cholecystokinin-pancreozymin was not significantly modified by atropine. When pancreatic juice was diverted during the course of an intravenous atropine infusion, the first 1-hour peak of protein output was significantly decreased, but the following 2-hour period was increased, the sum of these 2 periods being similar in both conditions. The response to soybean trypsin inhibitor during recirculation was decreased as well as the first peak after diversion. During atropine infusion fluid secretion decreased more powerfully after 1 h diversion and after soybean trypsin inhibitor than during recirculation of pancreatic juice. It is suggested that during recirculation of pancreatic juice nonstimulated protein secretion is mostly (89%), and water secretion is partially controlled by cholinergic mechanisms. After soybean trypsin inhibitor stimulus and during the early phase following juice diversion protein secretion seems to be partly under the control of cholinergic mechanisms. However, during the latter phase following diversion, it is not so. Parasympathetic stimulation appears also to play a significant, although less important, role in fluid secretion.

Animals↗
PubMedDate not supplied

Rat pancreatic secretory response to intraduodenal infusion of elemental vs polymeric defined-formula diet.

Pancreatic protein and fluid secretion in response to intraduodenal infusion of polymeric and elemental liquid defined-formula diets were studied in conscious rats. Rats were prepared with chronic pancreatic, biliary, and duodenal cannulas and had their pancreatic secretions collected and continuously returned to the intestine during intraduodenal infusion with commercial liquid defined-formula diets. Ensure HN, a polymeric defined-formula diet containing intact protein, and two elemental diets, in which the protein component consisted of enzymatically hydrolyzed protein and free amino acids, were tested. Ensure HN strongly stimulated pancreatic protein and fluid secretion, causing a maximal 10-fold increase in protein secretion. In contrast, the elemental diets stimulated only 30% to 47% of the protein secretion caused by Ensure HN. Separate infusion of the fat, protein, and carbohydrate components of one elemental diet, RTF Elemental, showed that fat was the major stimulant, but the responses to the separate components were not significantly different from each other and none caused more than 50% of the response to the complete diet. The results demonstrate that defined-formula elemental diets are much less stimulatory for pancreatic enzyme secretion than defined-formula polymeric diets in rats. The probable explanation for this difference is the replacement of intact protein by hydrolyzed protein and amino acids in the elemental diets.

Animals↗
PubMed2005

Mosquito natriuretic peptide identified as a calcitonin-like diuretic hormone in Anopheles gambiae (Giles).

Mosquito natriuretic peptide (MNP), an uncharacterised peptide from the yellow fever mosquito, Aedes aegypti, acts via cyclic AMP to stimulate secretion of Na+-rich urine by opening a Na+ conductance in the basolateral membrane of Malpighian tubule principal cells. Corticotropin releasing factor (CRF)-related peptides and calcitonin (CT)-like diuretic peptides use cyclic AMP as a second messenger and were therefore considered likely candidates for MNP. BLAST searches of the genome of the malaria mosquito Anopheles gambiae, gave sequences for the CRF-related peptide Anoga-DH44 and the CT-like peptide Anoga-DH31, which were synthesised and tested for effects on Malpighian tubules from An. gambiae and Ae. aegypti, together with 8-bromo-cyclic AMP. The cyclic AMP analogue stimulated secretion of Na+-rich urine by An. gambiae Malpighian tubules, reproducing the response to MNP in Ae. aegypti. It also depolarised the principal cell basolateral membrane voltage (Vb) while hyperpolarising the transepithelial voltage (Vt) to a similar extent. Anoga-DH4) and Anoga-DH31 stimulated production of cyclic AMP, but not cyclic GMP, by Malpighian tubules of An. gambiae. Both peptides had diuretic activity, but only Anoga-DH31 had natriuretic activity and stimulated fluid secretion to the same extent as 8-bromo-cyclic AMP. Likewise, Anoga-DH31 reproduced the effects of cyclic AMP on tubule electrophysiology, whereas Anoga-DH44 initially hyperpolarised Vb and depolarised Vt, which is the opposite of the effect of Anoga-DH31. Anoga-DH44 and Anoga-DH31 were also tested for effects on fluid secretion and ion transport by Ae. aegypti tubules. As in An. gambiae, the CRF-related peptide Anoga-DH44 had a non-specific effect on the transport of Na+ and K+, whereas the CT-like peptide Anoga-DH31 specifically stimulated transepithelial Na+ transport. We conclude that the CT-like peptide Anoga-DH31 is the previously uncharacterised mosquito natriuretic peptide.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2006

Potential difference measurements of ocular surface Na+ absorption analyzed using an electrokinetic model.

PURPOSE: Corneal and conjunctival epithelia are capable of transcellular Na+ absorption and Cl- secretion, which drives water movement across these tissues. A recent study demonstrated with a new open-circuit potential difference (PD) technique that Cl- moves across the ocular surface in mice through Ca2+- and cAMP-sensitive Cl- channels, the latter pathway being the cystic fibrosis (CF) transmembrane conductance regulator (CFTR). The purpose of the present study was to identify transporting mechanisms involved in Na+ absorption and to develop a mathematical model of ocular surface ion transport to quantify the relative magnitudes of and electrochemical coupling among transporting processes. METHODS: PDs across the fluid-bathed ocular surface were measured in anesthetized wild-type and CF mice in response to Na+, Cl-, and K+ ion substitution and transporter agonists, inhibitors, and substrates. An electrokinetic model of the ocular surface epithelium was developed to simulate PD measurements, which involved computation of membrane potentials and cell [Na+], [K+], [Cl-] and volume from transporter activities and extracellular ion concentrations. RESULTS: Na+ replacement produced a 6 +/- 2-mV depolarization that was blocked by amiloride (K(i) 0.8 microM) and benzamil (Ki 0.2 microM). The Na+-dependent depolarization by amiloride was significantly greater in CF mice (19 +/- 3 mV). In wild-type mice, D-, but not L-glucose produced a phloridzin-sensitive, 4.1-mV hyperpolarization in the presence of Na+ and amiloride, with a Km for D-glucose of 2.5 mM. Glycine and L-arginine also produced Na+-dependent hyperpolarizations. The epithelial transport model accurately reproduced experimental PD measurements. CONCLUSIONS: PD measurements coupled with model computations defined quantitatively the roles of Na+ and Cl- transport processes in ocular surface ion and fluid secretion, and indicated that CFTR-dependent changes in apparent epithelial Na+ channel (ENaC) activity could be accounted for by electrochemical coupling, without requiring ENaC-CFTR interactions. The data and modeling also predicted significant enhancement of ocular surface fluid secretion by ENaC inhibitors and CFTR activators as possible therapies for dry eye syndromes.

Absorption↗
PubMed1987

Diuretic action and immunological cross-reactivity of corticotropin and locust diuretic hormone.

A functional similarity and immunological cross-reactivity between adrenocorticotrophic hormone (ACTH) and a locust diuretic hormone (DH) is reported. The functional similarity is expressed in that ACTH mimics DH by stimulating fluid secretion and cyclic AMP (cAMP) secretion in locust Malpighian tubules. Desacetyl-alpha-melanocyte-stimulating hormone is active to a lesser degree but no other POMC-derived peptide tested was found to follow suit. Immunological cross-reactivity is shown by a positive response of HPLC-purified DH with a specific ACTH radioimmunoassay as well as a significant reduction in DH activity (fluid secretion) after incubations with ACTH antiserum. However, ACTH and DH are different peptides since they do not share common separation characteristics on HPLC and ACTH does not induce a high excess secretion of cAMP by the tubule cell as does DH.

Adrenocorticotropic Hormone↗
PubMed2000

Effect of helicokinins and ACE inhibitors on water balance and development of Heliothis virescens larvae.

The diuretic activity of the helicokinins I (YFSPWG-amide), II (VRFSPWG-amide) and III (KVKFSAWG-amide) was tested on Heliothis virescens larvae. All three kinins increased fluid secretion in isolated Malpighian tubules in a dose-dependent manner. Injections into the haemolymph caused a significant reduction in weight gain after 24 h and, in the case of helicokinin I, led to an increased mortality of 43% within 6 days. When truncated analogues of helicokinin I were tested in vitro, only the pentapeptide (FSPWG-amide) stimulated fluid secretion. Tested in vivo the pentapeptide did not influence normal development of the larvae. An alanine scan of helicokinin I showed that the substitution of phenylalanine, tryptophan and glycine led to a massive decrease or even loss of diuretic activity. The substitution of the other amino acids had no effect in vitro. The ACE inhibitors captopril, enalapril-maleate and lisinopril were tested for their influence on the development of the larvae. In combination with one of the helicokinins the in vivo injection of the ACE inhibitors led to increased rates of mortality and/or reductions in pupal weight.

Journal Article↗
PubMed2001

Lack of small intestinal ulcerogenecity of nitric oxide-releasing indomethacin, NCX-530, in rats.

AIM: To evaluate the intestinal ulcerogenic property of nitric oxide-releasing indomethacin (NCX-530) in the rat, in comparison with indomethacin. METHODS: Animals were given indomethacin or NCX-530 subcutaneously and killed 24 h later for macroscopic examination of the small intestine. RESULTS: A single administration of indomethacin (10 mg/kg) provoked damage, mainly in the jejunum and ileum, accompanied by an increase in myeloperoxidase and inducible nitric oxide synthase activities as well as bacterial translocation. NCX-530 at an equimolar dose (14.2 mg/kg) caused no gross damage in the small intestine, nor any significant change in inducible nitric oxide synthase and myeloperoxidase activities or bacterial translocation. NOR-3, the nitric oxide donor (6.0 mg/kg), when administered subcutaneously together with indomethacin, significantly prevented the occurrence of intestinal lesions and other mucosal changes. Indomethacin reduced mucus and fluid secretions in the small intestine, while both NCX-530 and NOR-3 enhanced these secretions. NCX-530 reduced the mucosal prostaglandin E2 contents and exhibited an anti-inflammatory action against carrageenan-induced paw oedema, with equal effectiveness to indomethacin. CONCLUSION: NCX-530 does not cause intestinal damage, despite inhibiting cyclooxygenase activity. The reduced intestinal toxicity of NCX-530 may be attributable to inhibition of enterobacterial translocation, partly by increasing the mucus and fluid secretions mediated by nitric oxide released from this compound.

Acetates↗
PubMed2001

Involvement of nerves and calcium channels in the intestinal response to Clostridium difficile toxin A: an experimental study in rats in vivo.

BACKGROUND: The involvement of nerves and calcium channels in the intestinal response to Clostridium difficile toxin A (luminal concentration 1 or 15 microg/ml) was studied in the small intestine of rats in vivo. METHODS: Inflammation was quantified by estimating myeloperoxidase (MPO) activity in the intestinal lumen, extravascular accumulation of Evan's blue (EB) in the intestine, and number of red blood cells (RBCs) in veins in histological sections. Intestinal damage was estimated using a histological grading system. In some experiments net fluid transport was recorded using a gravimetric technique. RESULTS: In acutely denervated intestines, toxin A caused marked destruction of the villi, increased luminal release of MPO activity, and augmentation of intestinal content of EB and venous RBCs. Denervating the intestine 3-4 weeks prior to the actual experiment prevented the development of villus damage and significantly decreased the number of RBCs in intestinal veins in experiments with a low toxin concentration, whereas no effect was demonstrated on luminal MPO activity. Using a high toxin concentration, chronic denervation decreased only the number of RBCs. Pretreatment with hexamethonium (low toxin concentration; acute denervation) attenuated the effect of toxin A on morphology, luminal MPO activity, and number of RBCs. Pretreatment with nifedipine (low toxin concentration; acute denervation) significantly decreased intestinal MPO activity and number of RBCs. Tissue accumulation of EB was not influenced by experimental manipulation. Net fluid transport was measured in experiments exposing the intestinal mucosa to a high toxin concentration. Fluid secretion caused by the toxin was significantly attenuated by intravenous hexamethonium whereas no effect was observed after administration of nifedipine or granisetron. CONCLUSIONS: At a low toxin concentration, intramural reflexes are involved in the inflammatory response whereas axon reflexes contribute to tissue damage. At a high toxin concentration no nervous involvement in the toxin A response was demonstrated except for fluid secretion evoked by the toxin.

Animals↗