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Results for “Fluids and Secretions”

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At least 19 recordsLinked to original sources

PubMed1999

Fluid secretion by isolated Malpighian tubules of Drosophila melanogaster Meig.: effects of organic anions, quinacrine and a diuretic factor found in the secreted fluid.

Para-aminohippuric acid (PAH, 0.2 and 1 mmol l(-)(1)) had no effect on the basal fluid secretion rate (FSR) of isolated Malpighian tubules of Drosophila melanogaster Meig. and did not affect stimulation of the FSR induced by adenosine 3',5'-monophosphate (cAMP). Phenol Red (phenolsulphonphthalein, PSP; 0.5 and 1 mmol l(-)(1)) slowed the FSR and abolished stimulation of the FSR by cAMP. Diodrast (1 mmol l(-)(1)) slightly, but significantly, reduced the FSR and greatly reduced the stimulation of the FSR normally provoked by cAMP and by the 3',5'-monophosphates of guanosine (cGMP), inosine (cIMP) and uridine (cUMP). However, stimulation of the FSR by the 3', 5'-monophosphate of cytidine (cCMP) was little affected by diodrast. Probenecid (0.2 or 1 mmol l(-)(1)) consistently stimulated the FSR, on average by approximately 25 %, but did not markedly inhibit the subsequent stimulation of the FSR by cAMP, cGMP or cIMP. However, the FSR of tubules stimulated by cGMP was temporarily lowered by probenecid. Quinacrine (0.1 mmol l(-)(1)) slowed basal FSR by an average of approximately 30 %, but subsequent stimulation of the FSR by cAMP was not noticeably affected. Both 0.1 mmol l(-)(1) cAMP and 1 mmol l(-)(1) probenecid stimulated adenylate cyclase activity in extracts of Malpighian tubules, but cIMP, cGMP, cUMP and diodrast were without effect in this regard. Uptake of radioactivity from a solution containing 500 nmol l(-)(1) [(3)H]cAMP and 9.5 micromol l(-)(1) cAMP was reduced by more than 90 % by 1 mmol l(-)(1) PSP, by approximately 40 % by 0.2 mmol l(-)(1) probenecid, by 36 % by 1 mmol l(-)(1) diodrast and by 30 % by 1 mmol l(-)(1) PAH. Neither 0.01 mmol l(-)(1) ouabain nor 0.1 mmol l(-)(1) quinacrine affected the uptake of [(3)H]cAMP by the Malpighian tubules. Fluid secreted by isolated Malpighian tubules of Drosophila melanogaster contains a factor that stimulated the FSR on average by approximately 50 %. The presence in the secreted fluid of cGMP at a concentration of 8.3 micromol l(-)(1) did not explain the stimulatory effect on FSR. These results support the existence of a carrier-mediated uptake of cyclic nucleotides into the Malpighian tubules of Drosophila melanogaster, possibly involving a multispecific transporter.

Adenylyl Cyclases↗

PubMed1995

Anion secretion drives fluid secretion by monolayers of cultured human polycystic cells.

We have investigated the hypothesis that active anion transport drives fluid secretion by the cystic epithelium in autosomal dominant polycystic kidney disease (ADPKD). We prepared monolayers of a primary culture derived from cystic tissue removed from ADPKD patients. The monolayers were grown on permeant supports, and fluid secretion was initiated by forskolin. The results were compared with those obtained with monolayers of Madin-Darby canine kidney (MDCK) cells, known to secrete Cl-. In the absence of the agonist, ADPKD monolayers absorbed fluid (0.20 +/- 0.02 microliter.cm surface area-2.h-1). Forskolin reversed this to secretion (0.60 +/- 0.03 microliter.cm-2.h-1). Control MDCK monolayers did not transport fluid in either direction, but forskolin induced secretion (0.48 +/- 0.03 microliter.cm-2.h-1). The electrical properties of the monolayers were monitored in Ussing chambers. Forskolin increased the transepithelial potential difference (Vte) of ADPKD monolayers (-0.9 +/- 0.1 to -1.1 +/- 0.1 mV) and the short-circuit current (Isc) (6.6 +/- 0.7 to 9.2 +/- 0.8 microA/cm2). The transepithelial resistance (Rte) fell (156 +/- 9 to 138 +/- 10 omega.cm2). Similar results were obtained with MDCK monolayers. The polarity of Vte and the direction of the Isc are compatible with the hypothesis that active secretion of anion drives fluid secretion. Basolateral application of the Na-K-2Cl cotransporter, bumetanide, reduced forskolin-stimulated fluid secretion by ADPKD monolayers (0.56 +/- 0.05 to 0.28 +/- 0.03), depolarized Vte, and inhibited Isc without affecting Rte. Apical application of the Cl- channel blocker, diphenylamine-2-carboxylate, also inhibited fluid secretion by ADPKD monolayers (0.65 +/- 0.03 to 0.27 +/- 0.02 microliter.cm-2.h-1).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMedDate not supplied

Mechanism and control of fluid secretion.

Fluid secretion and reabsorption by a variety of plant and animal tissues appear to be accomplished by osmotic coupling between solute transport and water movement. The local osmosis model suggests that active accumulation of solutes within narrow folds at the cell surface may produce the local gradients that generate water flow. Both micropuncture techniques and electron-probe X-ray microanalysis have established that local osmotic gradients occur in absorptive epithelia, but they have not as yet been detected in secretory tissues.Hormonal control of secretion involves stimulation of solute pumps and adjustments of permeability to non-transported solutes. Since hormone receptors and pumps are often located on opposite surfaces of the cell, intracellular second messengers convey the secretory signal through cytoplasm. Much has been learned by study of insect tissues that are anatomically simple and that function for long periods in vitro. Aspects of hormone-receptor interaction have been explored, including the action of halluninogenic molecules. In insect salivary glands cyclic AMP appears to stimulate cation transport, while calcium increases anion permeability. The various second messengers probably interact with each other in complex feedback loops that stabilize the system and make it quickly responsive to hormone. Cyclic AMP may stimulate release of calcium from mitochondria. Unresolved is the way second messengers alter properties of the cell surface.

Animals↗

PubMed1981

Ionic currents across pancreatic acinar cell membranes and their role in fluid secretion.

Fluid and enzyme secretion from a number of mammalian exocrine glands is controlled by the action of neurotransmitters and hormones on acinar cell membranes. Sustained stimulation evoking sustained fluid and enzyme secretion also evokes sustained membrane depolarization and increase in conductance. Mouse and rat pancreatic fluid and enzyme secretion, as well as membrane depolarization and conductance increase evoked by sustained stimulation with acetylcholine or cholecystokinin-gastrin peptides, are acutely dependent on extracellular calcium. However, the initial stimulant-evoked conductance increase and secretion appear to be triggered by calcium released from inside the cells. Direct measurement of membrane current during sustained stimulation in voltage-clamp experiments with resolution of the total current into its Na, Cl and K components has allowed calculations of stimulant-evoked Na and Cl uptake into the acinar cells. The NaCl uptake is quantitatively sufficient to account for the stimulant-evoked fluid secretion. The role of the stimulant-evoked transmembrane ionic current appears to be the supply of salt for the fluid secretion. Calcium derived from intracellular sources in the initial phase of secretion, and from the extracellular fluid in the sustained phase, couples fluid and enzyme secretion to hormone-receptor interaction.

Bicarbonates↗

PubMed1980

The role of sodium ions in pancreatic fluid secretion in the rabbit.

1. NaCl in the bathing medium of the isolated rabbit pancreas has been gradually replaced by isotonic amounts of either sucrose, choline chloride or KCl. 2. The replacement of NaCl always leads to a reduction in pancreatic flow. This reduction is largest with sucrose as replacing agent and smallest with KCl. 3. The Na+ concentration in the secreted fluid decreases only slightly when NaCl is replaced by sucrose. In the experiments with choline chloride, the Na+ concentration in the secreted fluid decreases slightly when less than 60 mM-NaCl has been replaced, but decreases markedly after more extensive NaCl replacement. Upon replacement of NaCl by KCl, the Na+ concentration in the secreted fluid is always equal to that in the bathing medium. 4. The K+ concentration in the secreted fluid increases by 8 mM upon replacing NaCl by either sucrose or choline chloride. Upon replacement by KCl the K+ concentration in the secreted fluid is always approximately equal to that in the bathing medium. 5. There is a linear relationship between the ratio of the K+ concentrations in the secreted fluid and the bathing medium and the ratio of the Na+ concentrations in these fluids. 6. Replacement of NaCl in the bathing medium does not lead to a change in the transepithelial potential. 7. The secreted fluid is always isotonic with that of the bathing medium; in the case of an extensive replacement of NaCl by either sucrose or choline chloride isotonicity is maintained by a higher cation concentration and an increased appearance of the replacing agents in the secreted fluid. 8. These studies confirm previous findings that extracellular Na+ is essential for pancreatic fluid secretion. 9. They also indicate that the monovalent cations reach the secreted fluid through a paracellular pathway. 10. These findings are incorporated in a model for the electrolyte movements involved in the pancreatic fluid secretion by ductular as well as by acinar cells.

Animals↗

PubMed1996

Chloride and fluid secretion by cultured human polycystic kidney cells.

Epithelial cells cultured from the renal cysts of patients with autosomal dominant polycystic kidney disease (ADPKD) secrete fluid via a process stimulated by adenosine 3',5'-cyclic monophosphate (cAMP). We have investigated the hypothesis that fluid secretion by these cells is dependent on cAMP-mediated chloride secretion. Individual cultured ADPKD cells were suspended within a polymerized collagen matrix and stimulated to form cysts. Individual cultured cysts were placed in a chamber on the stage of an inverted microscope equipped with epifluorescent and video analysis attachments. The rate of fluid secretion, cell volume and changes in intracellular Cl- were measured. In the absence of secretagogues, fluid was absorbed from the cyst cavity (-2.36 +/- 0.64 nl/min/cm2 inner surface area). 8-Bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) plus 3-isobutyl-1-methlyxanthine (IBMX) induced a rapid reversal in the net movement of fluid to secretion (6.79 +/- 1.28 nl/min/cm2). Bumetanide reversibly reduced fluid secretion to 0.95 +/- 0.60 nl/min/cm2. Cell volume rapidly decreased by 7.5 +/- 0.9% with the initiation of secretion and bumetanide caused an additional loss (4.2 +/- 1.0%). Furosemide had a similar effect on forskolin-induced fluid secretion. Cellular chloride concentration was monitored with the use of the indicator, 6-methoxy-N-ethylquinolinium chloride (MEQ). Removal of Cl- from the bath reduced intracellular [Cl-] (MEQ fluorescence increased by 11.4 +/- 2.3%). In cysts pretreated with furosemide to prevent Cl- entry, the application of forskolin caused a decrease in Cl- concentration (MEQ fluorescence increased by 9.3 +/- 2.6%). Using monolayers of cultured ADPKD cells, grown on permeant supports, we compared the changes in short circuit current (ISC) induced by forskolin in the presence and absence of external Cl-. Forskolin increased ISC (from 8.9 +/- 2.7 to 10.6 +/- 2.7 microA/cm2) in the presence of Cl-, but did not significantly affect ISC in its absence. These data indicate that cultured ADPKD cells can direct fluid transport in either the absorptive or the secretory direction, and that cAMP stimulates secretion and this secretion is accompanied by a net loss of cell solute. Inhibition of secretion by bumetanide or furosemide caused an additional loss of cell solute, including Cl-. The ionic transepithelial current induced by forskolin is dependent on the presence of Cl-. These data support the thesis that chloride secretion drives fluid secretion by cultured ADPKD cells.

Bumetanide↗

PubMed1996

Mechanism of fluid secretion common to aglomerular and glomerular kidneys.

Isolated renal proximal tubules of sea water fish net secrete fluid in vitro. The principal electrolytes in secreted fluid are Na, Cl, Mg and S. Transepithelial voltages may be lumen-negative or -positive by a few millivolts, and transepithelial resistances are low partly due to high paracellular Na and Cl permeabilities. Transepithelial electrochemical potentials indicate secretion of Mg into the tubule lumen by active transport. As Mg concentration in secreted fluid rises, Na concentration falls. Surprisingly, these observations of fluid secretion are made in glomerular and aglomerular proximal tubules, suggesting a fundamental mechanism common to both. Central to this commonality appears to be their behavior as open Donnan systems. Mg actively secreted into the tubule lumen from which it cannot diffuse back into the peritubular medium causes the transepithelial secretion of diffusible Na and Cl. Water follows by osmosis. Since there is flow out of the distal end of the tubule Donnan equilibrium is not attained. Instead, a dynamic Donnan system is maintained, driven by active transport of Mg. A mathematical model of tubular electrolyte and fluid secretion confirms the operation of this open, dynamic Donnan system in aglomerular and glomerular proximal tubules.

Animals↗

PubMed1994

Fluid secretion by isolated tick salivary glands dependent on an intact cytoskeleton.

Isolated salivary glands from female Dermacentor variabilis (Say) were pre-treated with either cytochalasin D or nocodazol, followed by stimulation with dopamine. Glands pre-treated with 1 microM-cytochalasin D did not secrete fluid; pre-treatment with 1 nM-cytochalasin D did not significantly reduce fluid secretion. Glands pre-treated with 1 microM-nocodazol had a significant reduction in fluid secretion (P = 0.003); 1 nM-nocodazol did not significantly affect fluid secretion. Ligation of the main salivary duct and pre-treatment with 1 microM-cytochalasin D significantly increased gland weight compared to the dopamine stimulated controls (P = 0.0412). Cytochalasin D-treated type III acini had a significantly larger mean diameter compared to the dopamine control (P = 0.0047). Glands treated with 1 mM-verapamil plus 10 microM-dopamine exhibited a significant decrease in fluid secretion (P = 0.017), and when ligated, had a significantly decreased weight compared to the controls (P = 0.0028).

Animals↗

PubMed1995

In vitro fluid secretion by epithelium from polycystic kidneys.

The size of the kidneys in patients with autosomal dominant polycystic kidney disease (ADPKD) is due in large measure to the accumulation of secreted fluid within thin-walled epithelial sacs. We measured the net transepithelial movement of liquid in response to forskolin in isolated, intact cysts excised from the surface of human ADPKD kidneys and in cultured, polarized monolayers of epithelial cells derived from ADPKD cysts. 10 excised cysts bathed symmetrically in control culture medium secreted fluid at a rate of 0.19 +/- 0.03 microliter/cm2 per hour after stimulation with forskolin (10 microM). Ouabain (100 microM) addition to the cavity fluid did not change the rate of fluid secretion of 10 forskolin-treated cysts, but addition of the glycoside to the external bathing medium fluid of nine cysts decreased secretion to -0.004 +/- 0.05 microliter/cm2 per hour. 24 monolayers absorbed fluid (range -0.029 to -0.412 microliter/cm2 per hour); by contrast, fluid was secreted (range 0.074 to 1.242 microliters/cm2 per hour) after stimulation with forskolin (10 microM). Ouabain (0.1 microM) in the basolateral but not in the apical medium inhibited fluid secretion. Forskolin increased the intracellular cyclic AMP content of ADPKD and MDCK monolayers by 236 and 196%, respectively. Six ADPKD monolayers had stable lumen negative transepithelial electrical potential differences (PDte) of -1.4 +/- 0.3 mV, positive short circuit currents (SCC) of 11.9 +/- 2.1 microAmp/cm2 and a tissue resistance (Rte) of 116 +/- 14 ohm.cm2. Forskolin increased SCC to 15.5 +/- 1.9 microAmp/cm2 (P < 0.005) and decreased Rte to 95 +/- 13 ohm.cm2 (P < 0.05); PDte remained stable at -1.4 +/- 0.3 mV. Ouabain (10 microM) had no effect when added to the apical medium, but in the basolateral medium decreased SCC to 1.7 +/- 0.3 microAmp/cm2 and PDte to -0.2 +/- 0.1 mV. We conclude that ADPKD cells in surface cysts have the potential to absorb or to secrete solutes and fluid. cAMP-mediated fluid secretion from the basolateral medium into the lumen of surface ADPKD cysts may be driven by anion transport.

Biological Transport↗

PubMed2003

Amino acids modulate ion transport and fluid secretion by insect Malpighian tubules.

Insect haemolymph typically contains very high levels of free amino acids. This study shows that amino acids can modulate the secretion of ions and water by isolated Malpighian tubules of Rhodnius prolixus and Drosophila melanogaster. Secretion rates of Rhodnius tubules in amino-acid-free saline increase after addition of serotonin to a peak value, then slowly decline to a plateau. Addition of glutamine, glutamate or aspartate to such tubules increases secretion rates dramatically relative to the controls in amino-acid-free saline, and these increases are sustained for 1-2 h. Seven other amino acids have more modest stimulatory effects, whereas lysine and arginine are inhibitory. Secreted fluid pH and Na(+) concentration increase and K(+) concentration decreases in response to glutamine. Pre-incubation of unstimulated tubules in saline solutions containing amino acids followed by stimulation with serotonin in amino-acid-free saline shows that the effects of amino acids far outlast the duration of exposure to them. Amino acids do not appear to be important as metabolites in Rhodnius tubules, nor do they act to draw significant amounts of water into the lumen by osmosis. Significant stimulation of fluid secretion can be achieved by physiological levels of particular amino acids, whereas those amino acids that inhibit fluid secretion only do so at concentrations much above those at which they occur naturally in the haemolymph. Secretion rates of unstimulated or stimulated Drosophila tubules are increased by pre-incubation in saline solutions containing glutamine or methionine or by continuous exposure to glutamine, methionine or tyrosine. Cysteine dramatically inhibited fluid secretion by Drosophila tubules, but only at concentrations well above the physiological range. We suggest that the amino acids probably function as compatible intracellular osmolytes that are necessary for sustained secretion at high rates by the Malpighian tubules.

Amino Acids↗

PubMed1994

Coupling of cell volume and membrane potential changes to fluid secretion in a model of renal cysts.

Renal tubular epithelia ordinarily absorb NaCl and water, although recent evidence indicates that renal cysts secrete fluid. We have utilized the experimental advantages offered by cultured cysts, formed in a collagen matrix by propagating Madin-Darby canine kidney cells, to investigate the mechanisms involved in fluid secretion by this renal epithelium. The rate of fluid transport (adduced from changes in cavity volume), cell volume and changes in membrane potential were measured simultaneously in isolated cysts. Under basal conditions, cysts absorbed fluid (-0.83 +/- 0.34 x 10(-6) ml/min/cm2 cavity surface area, N = 23). AVP and IBMX changed the direction of net fluid transport to secretion (4.24 +/- 0.49 x 10(-6) ml/min/cm2). Cell volume initially fell 7.4 +/- 0.5% and remained stable thereafter as secretion continued. Membrane electrical potential (bis-oxonol epifluorescence) hyperpolarized in 13 cysts and depolarized in 6, the mean change was 1.9 +/- 3.1%. Fluid secretion was abolished by 0.1 mM ouabain. Secretion was not affected by 0.1 mM DIDS and cell pH (bis-carboxyethyl-carboxyfluorescein epifluorescence) was not altered by the induction of secretion, suggesting that secretion is not dependent on Cl-HCO3 exchange. Barium, in the presence of AVP and IBMX, depolarized the cell membrane potential (bis-oxonol fluorescence increased 22.3 +/- 0.03%), reversed secretion to absorption (from 3.21 +/- 0.93 to -1.52 +/- 0.61 x 10(-6) ml/min/cm2), and increased cell volume 2.7 +/- 0.5%. Bumetanide (100 microM) reduced fluid secretion from 4.49 +/- 1.23 to -0.75 +/- 0.55 x 10(-6) ml/min/cm2, further reduced cell volume 4.4 +/- 1.2% and hyperpolarized the membranes (bis-oxonol fluorescence fell 24.3 +/- 5.0%). In the absence of AVP and IBMX bumetanide had no effect on fluid transport, cell volume or membrane potentials. We conclude that AVP reversed the direction of fluid transport in these cultured renal epithelial cysts from absorption to secretion by stimulating a coordinated interaction of basolateral and apical K, Cl and Na transport mechanisms.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗

PubMed1984

Arachnoid cysts of the sylvian fissure. Evidence of fluid secretion.

Morphological and enzyme ultracytochemical evidence is presented to support the contention that the walls of arachnoid cysts secrete fluid. Clinical evidence has already suggested this phenomenon, including intracranial pressure elevation and expansion in some cases, and the observation that arachnoid cysts constitute closed compartments with a fluid content that cannot be derived from other cerebrospinal fluid-containing spaces. Ultrastructurally, the cyst lining showed a similarity to subdural neurothelium and the neurothelial lining of arachnoid granulations in such morphological features as intercellular clefts with sinusoid dilatations, desmosomal intercellular junctions (upon which tonofilaments may be abutting), pinocytotic vesicles, multivesicular bodies, lysosomal structures, and the presence of a basal lamina. Some of these features, together with the presence of microvilli on the luminal surface, are consistent with fluid secretion. Moreover, enzyme cytochemistry demonstrated (Na+ + K+)-ATPase in the plasma membranes lining the cavity, either directly (the apical membranes), or via the intercellular clefts (the basolateral membranes), and, with alkaline phosphatase occupying the opposite plasma membranes, this structural organization indicates fluid transport toward the lumen. It may be surmised that arachnoid cysts derive from subdural neurothelium differentiating towards arachnoid villus mesothelium.

Adenosine Triphosphatases↗

PubMed1981

Potentiation by spiperone and other butyrophenones of fluid secretion by isolated salivary glands of ixodid ticks.

Isolated salivary glands from the ixodid tick, Amblyomma hebraeum Koch are stimulated to secrete fluid when exposed to dopamine (DA), the maximum response occurring at 10(-6) M. Spiperone, and a number of other butyrophenone derivatives, although lacking intrinsic activity, are able to potentiate the secretion elicited by supramaximal concentrations of DA; this potentiation by spiperone is evident at concentrations in the femtomolar range. Tranylcypromine, a potent, competitive inhibitor of monoamine oxidase (MAO) in tick salivary gland homogenates, has both intrinsic activity and potentiates DA-induced salivation. The fact that spiperone potentiates ergometrine-induced salivation that the prime mechanism of the butyrophenone effect is not by inhibiting catecholamine catabolism. The results also suggest that the receptor for DA and that for butyrophenones are distinct sites. Droperidol, benperidol and bromperidol, all potent neuroleptic drugs, failed (at 10(-9) M) to potentiate salivation. By contrast, R951, R27275 and R1187 (all at 10(-9) M) were very effective potentiators on the salivary gland system, despite the fact that they lack the basic structural requirements for neuroleptic activity. These results suggest that the butyrophenone site in tick salivary glands is different from butyrophenone binding sites in mammalian CNS.

Animals↗

PubMed1976

The influence of various factors on fluid secretion by in vitro salivary glands of ixodid Ticks.

1. Salivary glands of the female ixodid tick, Dermacentor andersoni, secrete fluid in vitro when bathed in a slightly modified version of the mammalian tissue culture medium 'TC 199'. 2. Rate of salivation in vitro increases with progression of feeding, but there is no comparable increase in dry weight of the salivary glands during the early phase of engorgement. Engorged ticks secreted at only 25% the rate of 90-250 mg ticks, indicating that salivary gland degeneration has already begun in the very early post-engorgement stage. 3. A salivary gland stimulating factor can be detected in the nervous system but not in other tissues. 4. Male salivary glands secrete at only 1/20th the rate of female glands. Thus males probably do not use their salivary glands as osmoregulatory organs. 5. From the uniform lack of response to ACh and uniform response to DA in 7 ixodid tick species, it is suggested that the control of salivation is similar throughout the ixodid family.

Acetylcholine↗

PubMed1985

Mechanism of fluid secretion in isolated shark renal proximal tubules.

Renal proximal tubules from the glomerular Squalus acanthias were studied for evidence of fluid secretion by closing one end of isolated tubules and leaving the other end open so that secreted fluid could be collected. When tubules were bathed in shark Ringer, fluid secretion rate was 27.6 +/- 3.9 (SE) pl X min-1 X mm-1 (21 tubules). Dibutyryl cAMP stimulated fluid secretion 50% (P less than 0.02, n = 14), furosemide inhibited fluid secretion 50% (P less than 0.01, n = 6), and metabolic inhibitors blocked fluid secretion nearly 100%. Secreted fluid was slightly hyperosmotic to peritubular bath (P less than 0.01, n = 7) but Na, Cl, S, K, and Ca concentrations were not significantly different from bath concentrations (wavelength-dispersive spectroscopy, electron probe analysis). cAMP had no effect on secreted fluid composition, and in some tubules cAMP did not stimulate fluid secretion. In conjunction with previous data we propose that spontaneous fluid secretion is driven by secretion of NaCl. However, finding the mechanism of NaCl and fluid secretion in glomerular renal tubules offers new perspectives of some previously inexplicable phenomena in the renal physiology of fish.

2,4-Dinitrophenol↗

PubMed1989

A model for fluid secretion in the exocrine pancreas.

Fluid secretion by the isolated rabbit pancreas is strongly dependent on the presence of Na+ in the bathing medium. Substitution of Na+ by another cation such as Li+ or K+ causes an inhibition of fluid secretion rate and a change in the composition of the secreted fluid which is dependent on the nature of the substituent cation. Stimulation of the pancreas by CCK-8 or carbachol increases paracellular ion permeability and, in some cases, also fluid secretion rate. We present a simple, quantitative model for ion and water secretion which accounts for the effects observed upon Na+ substitution and stimulation. The main features are active, Na+-dependent transcellular HCO3- transport and passive, paracellular cation and anion permeation. The activity of the HCO3- pump is dependent on the energy status of the cell and on the Na+ concentration in the bathing medium, and is competitively inhibited by K+. The paracellular ion permeabilities can be modulated by stimulatory agonists. We examine the extent to which, according to the model, fluid secretion is controlled by the various system parameters such as ion permeabilities and ion pump activity, and by external parameters such as the ion concentrations in the bathing medium. In addition, calculation of the effects of changes in these parameters are carried out in order to gain more insight in the mechanisms of secretion.

Animals↗

PubMed1986

Loperamide inhibits gallbladder inflammatory fluid secretion in experimental cholecystitis.

Fluid secretion by the gallbladder mucosa is suggested to have a key pathophysiological role in acute cholecystitis, since it causes distension of the obstructed gallbladder. The present study investigates the actions of loperamide on the gallbladder function in experimental cholecystitis. Gallbladder fluid transport and motility were studied in vivo with a continuous perfusion technique. A net fluid secretion by the gallbladder mucosa was seen in cats in which cholecystitis was induced whereas there was a net fluid absorption from the gallbladder lumen in the control animals. The net fluid secretion in experimental cholecystitis was inhibited by loperamide (1 mg/kg), an effect that was blocked by naloxone (1 mg/kg), suggesting an involvement of specific opiate receptors. Loperamide (1 mg/kg) relaxed the normal gallbladder but had no significant effects on its fluid absorption. Since loperamide reduces mucosal fluid secretion in experimental cholecystitis without contracting the gallbladder wall, it is suggested that this peripherally acting opiate agonist could be useful in the treatment of patients with acute cholecystitis.

Animals↗

PubMed1989

Role of monovalent cations in fluid secretion from the exocrine rabbit pancreas.

The role of Na+ in fluid secretion by the isolated rabbit pancreas was investigated. The fluid secretion rate is reduced upon replacement of Na+ in the bathing medium by Li+, K+ or choline. The inhibition depends on the nature of the substituting cation, and is largest with choline. Upon replacement, the substituent cation appears in the secreted fluid, and the Na+ concentration in the secreted fluid is decreased in a mirror-like fashion. When Na+ is replaced by Li+ or choline, the secretory Na+ concentration is decreased, although less than in the bathing medium, and the K+ concentration is increased. When Na+ is replaced by K+, the Na+ and the K+ concentration in the secreted fluid are approximately equal to their bathing medium concentrations. In the Li+ and choline medium, stimulation of the pancreas by carbachol or CCK-8 increases the fluid secretion rate. In addition, it increases the Li+ or choline concentration, and decreases the Na+ and K+ concentrations in the secreted fluid. In normal and K+ medium, stimulation causes only a slight increase in fluid secretion rate, with no change in the secretory Na+ concentration. In normal medium, stimulation leads to a decrease in the secretory K+ concentration. The effects of replacing Na+ appear to be the result of a direct inhibition of the active HCO3- transport underlying secretion, and an indirect inhibition related to the permeability of the pancreas for the various cations. The stimulants are likely to act by increasing the permeability of the tight junctions.

Animals↗