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At least 721 records · Page 40Linked to original sources
PubMed1989

Mechanism of action of calcitonin on secretion in rat submandibular gland.

Calcitonin (CT) was found to reduce the initial flow of pilocarpine-stimulated saliva from the submandibular glands in the rat. Although there was a concomitant increase of the concentration of calcium and protein in the saliva, the calcium/protein ratio was not significantly affected. CT also caused a significant increase of the potassium concentration in submandibular saliva. Both in vivo and in vitro, CT inhibited the production of cyclic AMP (cAMP) both in the absence and in the presence of forskolin. This decrease in intracellular cAMP levels could result in an inhibition of mucus secretion, which would explain the previously observed calcitonin-induced intracellular accumulation of mucus in the submandibular gland acinar cells. CT did not affect the cytoplasmic free Ca2+ concentration (as measured with fura 2) in isolated submandibular acini either in the absence or in the presence of cholinergic or adrenergic agonists. These results indicate that the inhibition of fluid secretion in the submandibular gland by calcitonin must be located distal to changes in [Ca2+]i. It can be concluded that CT affects both mucus and fluid secretion in the submandibular gland, but that only the inhibition of mucus secretion can as yet be explained by an effect at the level of the second messenger.

Adenylyl Cyclases↗
PubMed1997

Role of intestinal epithelial cells in the host secretory response to infection by invasive bacteria. Bacterial entry induces epithelial prostaglandin h synthase-2 expression and prostaglandin E2 and F2alpha production.

Increased intestinal fluid secretion is a protective host response after enteric infection with invasive bacteria that is initiated within hours after infection, and is mediated by prostaglandin H synthase (PGHS) products in animal models of infection. Intestinal epithelial cells are the first host cells to become infected with invasive bacteria, which enter and pass through these cells to initiate mucosal, and ultimately systemic, infection. The present studies characterized the role of intestinal epithelial cells in the host secretory response after infection with invasive bacteria. Infection of cultured human intestinal epithelial cell lines with invasive bacteria, but not noninvasive bacteria, is shown to induce the expression of one of the rate-limiting enzymes for prostaglandin formation, PGHS-2, and the production of PGE2 and PGF2alpha. Furthermore, increased PGHS-2 expression was observed in intestinal epithelial cells in vivo after infection with invasive bacteria, using a human intestinal xenograft model in SCID mice. In support of the physiologic importance of epithelial PGHS-2 expression, supernatants from bacteria-infected intestinal epithelial cells were shown to increase chloride secretion in an in vitro model using polarized epithelial cells, and this activity was accounted for by PGE2. These studies define a novel autocrine/paracrine function of mediators produced by intestinal epithelial cells in the rapid induction of increased fluid secretion in response to intestinal infection with invasive bacteria.

Animals↗
PubMed1986

Effects of cyclic nucleotide derivatives on acetylcholine-induced secretion from isolated, perfused rat submandibular salivary glands.

The effects of dibutyryl cAMP, 8-bromo-cGMP, 3-isobutyl-1-methyl xanthine (MIX) and isoproterenol were examined. When administered simultaneously with acetylcholine (10(-6) M) in concentrations of 10(-5) M, both isoproterenol and cAMP reduced fluid secretion (16 and 31 per cent, respectively) and enhanced the decay in rate of flow with time, while cGMP and MIX increased salivary volumes (25 and 19 per cent, respectively). Isoproterenol-decreased Na and Cl and increased K and residual anion concentrations. These effects, except for increased K, were also observed with MIX, cAMP and cGMP did not significantly affect cation concentrations but reduced Cl and increased residual anion, although to a lesser extent than isoproterenol or MIX. The cyclic nucleotides did not affect the flow of saliva when added to the perfusate for 40 min after 40 min of acetylcholine stimulation. Prior exposure to cGMP increased the volume of saliva secreted after re-exposure to acetylcholine alone and both cGMP and cAMP increased the Na and reduced the K concentration of the stimulated secretion. These results suggest that cyclic nucleotides are involved in salivary fluid and electrolyte secretion and can modulate the effects of cholinergic stimuli. cGMP may be involved mainly in fluid secretion and, as salivary fluid originates almost exclusively in salivary acini, it may exert its action in acinar cells and activate specific components of the mechanism of primary secretion. cAMP may be primarily involved in transductal electrolyte transport, and may also inhibit certain parts of the fluid secretory mechanism, or reduce the effectiveness of cholinergic stimuli in activating them.(ABSTRACT TRUNCATED AT 250 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed1975

Secretory activity and aryl acid content of serum, urine, and cerebrospinal fluid in normal and uremic man.

Serum from uremic human subjects causes net fluid secretion in proximal straight tubules isolated from rabbit kidneys in a manner similar to paraaminohippuric acid. In the present study, we determined the relation between the concentration of aryl acids (hippuric acid, benzoic acid, etc.) In serum, urine, and cerebrospinal fluid (CSF) and the capacity of the biologic fluids to cause fluid secretion in renal tubules. The concentration of aryl acids in serum and urine as estimated by fluorometric assay (Fl-Hipp) was related to the secretory activity (SA) estimated by bioassay in a direct linear fashion over a 10,000-fold range of concentrations. Fl-Hipp and SA were strikingly elevated in the serum of uremic patients. Hippuric acid determined by gas-liquid chromatography accounted for approximately one-fourth of the secretory activity of serum and urine; benzoic acid was present only in trace amounts; the remainder of the secretory activity of uremic serum is probably due to derivatives of aryl acids which are detected as Fl-Hipp. The relation between creatinine clearance and the SA or Fl-Hipp concentration of serum was hyperbolic; both the SA and Fl-Hipp content of serum increased sharply when creatinine clearance fell below 10 ml. per minute. The SA and Fl-Hipp content of CSF was increased in uremic patients; however, the serum content exceeded that of the CSF by more than fourfold suggesting an exclusion mechanism for aryl acids in the central nervous system. We conclude that the secretory activity of uremic serum is due to the accumulation of aryl acids, probably of the hippurate class, and, further, that relatively high levels of these biologically active substances may contribute to general organ dysfunction in uremia owing to their potential to act as competitive inhibitors of organic anion transport.

Animals↗
PubMed2004

Conservation of capa peptide-induced nitric oxide signalling in Diptera.

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. The roles of NO synthase (NOS), NO and cGMP in capa peptide signalling were tested in several other insect species of medical relevance within the Diptera (Aedes aegypti, Anopheles stephensi and Glossina morsitans) and in one orthopteran out-group, Schistocerca gregaria. NOS immunoreactivity was detectable by immunocytochemistry in tubules from all species studied. D. melanogaster, A. aegypti and A. stephensi express NOS in only principal cells, whereas G. morsitans and S. gregaria show more general NOS expression in the tubule. Measurement of associated NOS activity (NADPH diaphorase) shows that both D. melanogaster capa-1 and the two capa peptides encoded in the A. gambiae genome, QGLVPFPRVamide (AngCAPA-QGL) and GPTVGLFAFPRVamide (AngCAPA-GPT), all stimulate NOS activity in D. melanogaster, A. aegypti, A. stephensi and G. morsitans tubules but not in S. gregaria. Furthermore, capa-stimulated NOS activity in all the Diptera was inhibited by the NOS inhibitor l-NAME. All capa peptides stimulate an increase in cGMP content across the dipteran species, but not in the orthopteran S. gregaria. Similarly, all capa peptides tested stimulate fluid secretion in D. melanogaster, A. aegypti, A. stephensi and G. morsitans tubules but are either without effect or are inhibitory on S. gregaria. Consistent with these results, the Drosophila capa receptor was shown to be expressed in Drosophila tubules, and its closest Anopheles homologue was shown to be expressed in Anopheles tubules. Thus, we provide the first demonstration of physiological roles for two putative A. gambiae neuropeptides. We also demonstrate neuropeptide modulation of fluid secretion in tsetse tubule for the first time. Finally, we show the generality of capa peptide action, to stimulate NO/cGMP signalling and increase fluid transport, across the Diptera, but not in the more primitive Orthoptera.

Amino Acid Sequence↗
PubMed1980

Dose-related effects of chenodeoxycholic acid in the rabbit colon.

The effects of bile acid (BA) concentration on fluid secretion, mucus secretion, and mucosal damage were investigated during dose-response studies in the rabbit colon with 1, 2.5, and 5 mM sodium chenodeoxycholate (NaCDC). 1 mM NaCDC resulted in mucus secretion followed by mucosal damage but no change in fluid transport was observed. At 2.5 mM concentration, mucus secretion and mucosal damage were evident within 1 hr of perfusion whereas fluid secretion developed in the second hour only. At 5 mM concentrations, all changes occurred simultaneously. The magnitude of changes increased with the concentration of BA perfused. These results are consistent with the hypothesis that mucus secretion with loss of its cytoprotective effect precedes, and thus may permit, the detergent effects of the di-alpha-hydroxy bile acid on the mucosa, resulting in mucosal damage. Both these effects precede changes in fluid and electrolyte transport.

Animals↗
PubMed1992

Expression and characterization of the cloned Salmonella typhimurium enterotoxin.

Earlier, our laboratory reported the cloning of a chromosomally encoded cholera toxin (CT)-like enterotoxin gene from Salmonella typhimurium Q1 into pBR322. Cell lysates from the plasmid clone pC1, containing a 4.8 kb EcoR1 DNA fragment from Salmonella, caused elongation of Chinese hamster ovary (CHO) cells and this biologic activity was neutralized by anti-CT. However, this cloned gene product did not elicit fluid secretion in the rabbit intestinal loop (RIL) model, because of poor expression. We report here, subcloning of a 4.8 kb EcoRI and a 2.7 kb HindIII/Eco Rl fragment into a high expression T7 RNA polymerase/promoter system. Cell lysates from these clones elicited fluid secretion in the RIL model, caused firm induration in rabbit skin and elongated CHO cells. These biological activities were neutralized by anti-CT. SDS-PAGE and subsequent fluorographic analysis of Escherichia coli, harboring recombinant plasmids in a T7 expression system, revealed the presence of two prominent 35S-labeled polypeptides of 25 and 12 kDa, which were immunoprecipitated with anti-CT. The enterotoxin appeared to be 125 kDa in size, based on chromatography on a P-300 column, had a pl of 6.6 to 6.8, and was heat-labile (60 degrees C/5 min). Unlike cloned CT and heat-labile enterotoxin (LT-l), which were localized in the periplasm, the Salmonella enterotoxin was cytoplasmic in nature.

Animals↗
PubMed2004

Therapies to slow polycystic kidney disease.

Advances in the understanding of cystogenesis and availability of animal models orthologous to human autosomal dominant polycystic kidney disease (ADPKD) and recessive polycystic kidney disease (ARPKD) will likely facilitate the development of treatments for these diseases. Proteins mutated in ADPKD and ARPKD, as well as in several animal models, are localized to renal primary cilia. These are thought to have a sensory function and contribute to the regulation of the intracellular calcium ([Ca2+]i). It seems likely that the maintenance of a differentiated renal epithelial phenotype, characterized by controlled fluid secretion and cell proliferation, requires precise functional coordination of cAMP and Ras/Raf/MEK/ERK signaling by [Ca2+]i. [Ca2+]i alterations, linked to genetic defects causing polycystic kidney disease, may hinder negative feedback mechanisms that control cAMP and Ras/Raf/MEK/ERK signaling, and result in increased fluid secretion and cell proliferation. cAMP levels, Raf kinase activities and ERK phosphorylation are increased in polycystic kidneys. There is also evidence of abnormal cross-talk between cAMP and MAPK pathways, that can be reproduced in wild-type cells by altering [Ca2+]i. While cAMP inhibits Ras-Raf-1-stimulated phosphorylation of ERK in normal kidney cells, it markedly increases B-Raf kinase activity and ERK phosphorylation in polycystic kidney cells. Treatment strategies should probably be aimed at increasing [Ca2+]i, inhibiting Ras/Raf/MEK/ERK signaling or lowering cAMP in the distal nephron and collecting duct. Vasopressin is the major adenylyl cyclase agonist in the collecting duct principal cells via a V2 receptor. OPC31260, a V2 receptor antagonist, lowers renal cAMP and markedly inhibits cystogenesis in four animal models of polycystic kidney disease, three of which are orthologous to human diseases (PCK rat, ARPKD; pcy mouse, adolescent nephronophthisis; Pkd2WS25/- mouse, ADPKD). The renal selectivity and safety profile of this class of drugs make it an excellent candidate for clinical trials.

Animals↗
PubMed2000

Aquaporin water channel in salivary glands.

Water secretion from salivary glands, which are innervated by parasympathetic and sympathetic nerves, occurs in response to the stimulation by neurotransmitters. In general, parasympathetic or sympathetic stimulation produces a high flow of saliva as a result of the activation of M3 muscarinic or alpha1-adrenergic receptors, respectively. The secretory mechanisms of fluid secretion were osmotically regulated in response to a transepithelial ion gradient generated by ion transport systems that were located in the apical or basolateral membranes of the acinar cells. Recently, the identification of water-specific channels, or aquaporins (AQPs), in many mammalian tissue and cell types has provided insight into the molecular basis of water movement across biological membranes. It has been reported that several AQPs are expressed in salivary glands and especially AQP5 plays an important role in fluid secretion. This review will focus on the role of AQP5 in the movement of water across the apical plasma membrane in relation to the physiology and pathophysiology of salivary glands.

Animals↗
PubMed2002

Effect of inositol-trisphosphate on fluid transport and protein extravasation in the obstructed small bowel.

BACKGROUND: Small-bowel obstruction is characterized by accumulation of fluid in the obstructed intestine. A pronounced inflammation in the obstructed gut wall has been shown to play an important role in the pathogenesis of the profuse fluid losses. alpha-Trinositol (D-myo-inositol-1,2,6-trisphosphate; PP56) has potent anti-inflammatory as well as antisecretory properties. The effects of alpha-Trinositol on inflammation and fluid losses in the obstructed small intestine are examined. METHODS: A total obstruction of the proximal part of the rat jejunum was induced during 18 h by thread ligation. A small segment of the obstructed intestine, with intact vascular and nervous supply, was placed in a chamber suspended from a force displacement transducer allowing for continuous registration of net fluid transport on a Grass polygraph. Three groups were included. One group (n = 12) received low-dose alpha-Trinositol (bolus: 2 mg kg(-1); IV infusion: 10 mg kg(-1) min(-1)), a second group (n = 10) received high-dose alpha-Trinositol (bolus: 12 mg kg(-1); IV infusion: 60 mg kg(-1) min(-1)), while a control group (n = 9) received corresponding volumes of isotonic saline (bolus: 0.5 ml; IV infusions 15 microl min(-1)). Quantitative measurement of extra-vasated Evans blue albumin in the obstructed jejunum was used as a marker of inflammation. RESULTS: High-dose alpha-Trinositol induced a significant (P < 0.001) inhibition of net fluid secretion, while low-dose alpha-Trinositol had no significant effect versus saline. In contrast, both doses of alpha-Trinositol induced significant inhibition of EB-albumin leakage (P < 0.05). CONCLUSION: High-dose alpha-Trinositol is a potent inhibitor of fluid secretion in obstructive ileus, most probably involving an anti-inflammatory mechanism.

Animals↗
PubMed1989

Interaction between sympathetic nerve fibres and epithelial transport in the rat jejunal mucosa in vivo.

The aim of this study was to elucidate the mechanisms behind the absorptive response to mesenteric nerve stimulation (MNS). Segments of rat jejunum were mounted with intact blood circulation in an 'in-vivo chamber', allowing parallel registration of net fluid transport rate (NFT) and electrical parameters of the tissue. All segments secreted fluid spontaneously, and the secretion rate was inversely correlated to the corresponding potential difference (PD) across the segment. The secretion was not inhibited by atropine. The nicotinic antagonist hexamethonium (Hx) inhibited the secretion and changed the relationship between PD and NFT. MNS reversed the secretion into an absorption (absorptive response) and decreased PD and short-circuit current (SCC) (electrogenic response). Total tissue resistance (Rt) was not significantly changed. The absorptive response increased at high control secretion rates and the electrogenic response increased at high control PD levels. The electrogenic response was inversely related to the absorptive response; however, the presence of Hx reversed this correlation. Guanethidine, a sympatholytic agent, eliminated all effects of MNS. Phentolamine eliminated the absorptive response but not the electrogenic response, and the remaining electrogenic response was not sensitive to propranolol (a beta-adrenergic antagonist). Hx induced similar but smaller effects than MNS, and after Hx treatment the MNS effects were reduced. We conclude: (1) Fluid secretion in our model involves a mechanism other than electrogenic Cl- secretion. (2) MNS activates sympathetic nerve fibres, which enhance fluid absorption and decrease PD and SCC. (3) The absorptive and electrogenic responses involve partly separate transport mechanisms. (4) Both responses are partly due to the inhibition of intramural secretory nervous pathways. (5) Some sympathetic nerve fibres interact directly with the epithelium.

Adrenergic Fibers↗
PubMed1999

Acute oxidative stress modulates secretion and repetitive Ca2+ spiking in rat exocrine pancreas.

The effects of the oxidant tert-butylhydroperoxide (t-buOOH) on carbachol-stimulated pancreatic secretion in the vascularly perfused rat pancreas have been studied in parallel with [Ca2+]i signalling and amylase output in perifused rat pancreatic acinar cells. Perfusion of the pancreas with t-buOOH (0.1-1 mM) caused a rapid and irreversible inhibition of carbachol-stimulated (3x10-7 M) amylase and fluid secretion. Pre-perfusion of the pancreas with vitamin C and dithiothreitol or a cocktail of GSH and GSH-precursor amino acids provided only marginal protection against the deleterious effects of t-buOOH, even though GSH levels were elevated significantly. In perifused pancreatic acini, repetitive [Ca2+]i spikes evoked by carbachol (3x10-7 M) were sustained for 40 min. t-buOOH (1 mM) acutely increased the amplitude and duration of Ca2+ spikes, then attenuated Ca2+ spiking and subsequently caused a marked and sustained rise in [Ca2+]i. t-buOOH-induced alterations in carbachol-stimulated [Ca2+]i signalling and amylase release in perifused pancreatic acini were prevented by vitamin C. Although vitamin C restored impaired Ca2+ signalling and maintained amylase output in pancreatic acini, it seems likely that oxidative stress inhibits fluid secretion irreversibly in the intact pancreas, resulting in a loss of amylase output. Thus, perturbations in [Ca2+]i signalling may not fully explain the secretory block caused by oxidative stress in acute pancreatitis.

Amylases↗
PubMed1979

Ionic composition of small intestinal secretion induced by PGE2.

Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions.

Animals↗
PubMed1990

Elevation of [Ca2+]i and the activation of ion channels and fluxes by extracellular ATP and phospholipase C-linked agonists in rat parotid acinar cells.

Extracellular ATP initiates a variety of changes in the parotid acinar cell. The initial effect appears to be the entry of Ca2+ (and perhaps Na+), and a series of ion transport events result from the subsequent elevation of [Ca2+]i. Agonists of phospholipase C-linked receptors elevate [Ca2+]i by a different pathway, involving the generation of inositol polyphosphate compounds, but share in the subsequent initiation of the ion transport events. Although the maintenance of the physiological changes may depend on specific inositol polyphosphate intermediates, the critical initiating factor is the elevation of [Ca2+]i. Fluid secretion by the parotid gland is triggered by the action of neurotransmitters, which alter the membrane permeability of the acinar cell. The similarities between the two receptor-mediated activation pathways suggests that ATP may act as a neurotransmitter and play a role in the control of fluid secretion. Basing our analysis on the purinoceptor characteristics outlined by Gordon, we suggest that the parotid receptor belongs to the P2Z class, which is highly sensitive to ATP4-. Basing his analysis on the earlier report by Gallacher of the effects of ATP on mouse parotid cells, Gordon placed the parotid purinoceptor in a different P2 subclass (P2Y). However, our findings of an increased potency of ATP in the absence of Mg2+, as well as the potency order of different nucleotides, indicate that the P2Z class is a more appropriate category.

Adenosine Triphosphate↗
PubMed2005

Phenotype analysis of aquaporin-8 null mice.

Aquaporin-8 (AQP8) is a water-transporting protein expressed in organs of the mammalian gastrointestinal tract (salivary gland, liver, pancreas, small intestine, and colon) and in the testes, heart, kidney, and airways. We studied the phenotype of AQP8-null mice, and mice lacking AQP8, together with AQP1 or AQP5. AQP8-knockout mice lacked detectable AQP8 transcript and protein, and had reduced water permeability in plasma membranes from testes. Breeding of AQP8 heterozygous mice yielded AQP8-null mice, whose number, survival, and growth were not different from those of wild-type mice. Organ weight and serum/urine chemistries were similar in wild-type and AQP8-null mice, except for increased testicular weight in the null mice (4.8 +/- 0.7 vs. 7.3 +/- 0.3 mg/g body wt). Urinary concentrating ability in AQP8-null mice was unimpaired as assessed by urine osmolality (3,590 +/- 360 mosmol/kgH(2)O) and weight loss (22 +/- 2%) after 36-h water deprivation; urinary concentrating ability was similarly impaired in AQP1-null mice vs. AQP8/AQP1 double-knockout mice. Agonist-driven fluid secretion in salivary gland was not different in AQP8 vs. wild-type mice ( approximately 1 microl.min(-1).g body wt(-1)) or in AQP5-null mice vs. AQP8/AQP5 double-knockout mice. Closed intestinal loop measurements in vivo indicated unimpaired osmotically driven water transport, active fluid absorption, and cholera toxin-driven fluid secretion in AQP8-null mice. After 21 days on a 50% fat diet, wild-type and AQP8-null mice had similar weight gain ( approximately 15 g), with no evidence of steatorrhea or abnormalities in blood chemistries, except for mild hypertriglyceridemia in the null mice. The mild phenotype of AQP8-null mice was surprising in view of the multiple phenotype abnormalities found in mouse models of AQP1-5 deficiency.

Animals↗
PubMed1998

The action of inhibitors of protein kinases on fluid and ion secretion by Malpighian tubules of Locusta migratoria, L.

Fluid production in Locusta Malpighian tubules was stimulated by corpora cardiaca extract (c. 100%) and dibutyryl cAMP (c. 50%). Chelerythrine and staurosporine (Protein kinase C, PKC inhibitors) inhibited it in the range 0.07-60&mgr;M (IC(50)3&mgr;M), whereas Rp-cAMP (Protein kinase A, PKA inhibitor) caused inhibition over the concentration range 10-1000&mgr;M (IC(50)264&mgr;M). The protein phosphatase inhibitor, okadaic acid, was also inhibitory over the concentration range 0.1-1000nM (IC(50) 91nM). CC extract stimulation increased fluid [Na(+)] from 41 to 59mM and decreased [K(+)] from 127 to 107mM; stimulation with cAMP had no such effect. The PKC inhibitors reduced the [K(+)] in the secreted fluid from 126 to 107mM but had no effect on the [Na(+)]. Subsequent addition of CC extract stimulated fluid production and caused an increase in [Na(+)] from 41 to about 50mM. The addition of Rp-cAMP reduced fluid production but caused a decrease in [Na(+)] from 37 to 28mM and an increase in its [K(+)] from 124 to 148mM. Fluid production by Rp-cAMP inhibited tubules was not stimulated by corpora cardiaca extract or cAMP, but [Na(+)] rose to 36mM. Protein phosphorylation plays a role in the regulation of fluid production probably via the apical and basal membrane cation transporters.

Journal Article↗
PubMed2006

Evaluation of the antidiarrhoeal activity of Byrsocarpus coccineus.

Based on its use in traditional African medicine, the antidiarrhoeal activity of the aqueous leaf extract of Byrsocarpus coccineus, Connaraceae, was evaluated on normal and castor oil-induced intestinal transit, castor oil-induced diarrhoea, enteropooling and gastric emptying. The extract (50, 100, 200 and 400 mg/kg, p.o.) produced a significant (P<0.05) dose dependent decrease in propulsion in the castor oil-induced intestinal transit in mice. The mean peristaltic index (%) for these doses of extract, control (distilled water; 10 ml/kg, p.o.) and morphine (10 mg/kg, s.c.) were 55.27+/-1.86, 53.12+/-3.73, 38.60+/-3.79, 30.25+/-1.27, 89.33+/-5.62 and 20.29+/-3.38, respectively. The effect of the extract at the highest dose was significantly (P<0.05) lower than that of the standard drug. This effect was antagonised by yohimbine (1 mg/kg, s.c.) but not by isosorbide dinitrate (IDN, 150 mg/kg, p.o.). At 200 mg/kg, the extract produced a significant decrease in propulsion in normal intestinal transit. In a dose dependent manner, it delayed the onset of diarrhoea, produced a significant decrease in the frequency of defaecation, severity of diarrhoea and protected the mice treated with castor oil. Mean diarrhoea scores were 30.83+/-1.72, 22.40+/-1.71, 21.43+/-1.32, 13.80+/-0.33, 18.00+/-3.94 and 7.67+/-2.41 for control, extract (50, 100, 200 and 400 mg/kg) and morphine, respectively. This effect was not antagonized by IDN. The extract (400 mg/kg) significantly decreased the volume (ml) of intestinal fluid secretion induced by castor oil (0.60+/-0.23) compared with 1.27+/-0.12 for control. However, there was no significant effect on gastric emptying. The results obtained suggest that Byrsocarpus coccineus possesses antidiarrhoeal activity due to its inhibitory effect on gastrointestinal propulsion, mediated through alpha(2) adrenoceptors, and also inhibition of fluid secretion. Preliminary phytochemical analysis revealed the presence of alkaloids, tannins, saponins, reducing sugars, glycosides and anthraquinones.

Animals↗
PubMed1999

[Role of chloride 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↗