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PubMed2006

Gastrointestinal processing of Na+, Cl-, and K+ during digestion: implications for homeostatic balance in freshwater rainbow trout.

The role of the gastrointestinal tract in maintaining ionic homeostasis during digestion, as well as the relative contribution of the diet for providing electrolytes, has been generally overlooked in many aquatic species. An experimental diet that contained an inert reference marker (lead-glass beads) was used to quantify the net transport of Na(+), K(+), and Cl(-) during the digestion and absorption of a single meal (3% ration) by freshwater rainbow trout (Oncorhynchus mykiss). Secretion of Cl(-) into the stomach peaked at 8 and 12 h following feeding at a rate of 1.1 mmol.kg(-1).h(-1), corresponding to a theoretical pH of 0.6 in the secreted fluid (i.e., 240 mmol/l HCl). The majority ( approximately 90%) of dietary Na(+) and K(+) was absorbed in the stomach, whereas subsequent large fluxes of Na(+) and Cl(-) into the anterior intestine corresponded to a large flux of water previously observed. The estimated concentration of Na(+) in fluids secreted into the anterior intestine was approximately 155 mmol/l, equivalent to reported hepatic bile values, whereas the estimated concentration of Cl(-) ( approximately 285 mmol/l) suggested seepage of HCl acid from the stomach in advance of the chyme front. Net absorption of K(+) in the stomach occurred following the cessation of Cl(-) secretion, providing indirect evidence of K(+) involvement with HCl acid production. Overall, 80-90% of the K(+) and Cl(-) contents of the meal were absorbed on a net basis, whereas net Na(+) absorption was negligible. Chyme-to-plasma ion concentration gradients were often opposed to the direction of ion transport, especially for Na(+) and Cl(-).

Animals↗
PubMed1996

Separate control of anion and cation transport in malpighian tubules of Drosophila Melanogaster.

Microelectrode measurements of basal, apical and transepithelial potentials in the Malpighian tubules of Drosophila melanogaster were obtained under a range of conditions in order to investigate whether each of the three main second messenger systems known to act in the tubules (cyclic AMP, cyclic GMP and Ca2+) acted specifically on either cation or anion transport, or whether they activated both systems. Ion-selective microelectrode determinations of K+ concentration and pH of secreted fluid allowed the role of each signalling system to be analysed further. Stimulation with cyclic nucleotides markedly alters the potential profile across principal cells through the selective activation of an apical electrogenic V-ATPase. By contrast, manipulation of extracellular chloride levels, combined with stimulation with leucokinin, does not affect the potential profile across the principal cells, showing that chloride must pass through another route. The cell-permeant Ca2+ chelator BAPTA-AM was shown to suppress the action of leucokinins (insect peptides that induce rapid fluid secretion), but not those of cyclic AMP, the neuronally derived insect peptide cardioacceleratory peptide 2b (CAP2b) or its intracellular messenger cyclic GMP. This shows that leucokinins act through Ca2+ and not through cyclic nucleotides and that the cyclic nucleotide pathways do not co-activate the intracellular Ca2+ pathway to exert their effects. Taken together, these results show that leucokinin acts through intracellular Ca2+, independently of cyclic AMP or cyclic GMP, to raise the chloride permeability of the epithelium. By contrast, either cyclic AMP or cyclic GMP (upon CAP2b stimulation) acts on the electrogenic cation-transporting apical V-ATPase, with only a negligible effect on anion conductance and without perturbing intracellular [Ca2+]. There is thus a clear functional separation between the control pathways acting on cation and anion transport in the tubules. Given the evidence from D. melanogaster and other species that chloride does not pass through the principal cells, we speculate that these two pathways may also be physically separated within cell subtypes of the tubules.

Animals↗
PubMed1993

The secretion of fluid by renal cysts from patients with autosomal dominant polycystic kidney disease.

BACKGROUND: The mechanism by which fluid accumulates in renal cysts of adults with autosomal dominant polycystic kidney disease is not known. This study was designed to determine whether transepithelial secretion of fluid may account for this accumulation. METHODS: We studied in vitro intact cysts that were excised from kidneys removed from three patients with end-stage autosomal dominant polycystic kidney disease. The cysts were loaded with natural cyst fluid or with a combination of Dulbecco's modified Eagle's medium and Ham's F12 medium (DME-F12) and incubated in DME-F12 for 24 hours. Fluid secretion, determined by the change in the weight of the cysts, was expressed as the rate of fluid secretion per square centimeter of surface area per 24 hours, to correct for the wide variation in the sizes of the cysts. To test for endogenous secretagogues, cyst fluid was added to confluent monolayer cultures of canine- and human-kidney cells. RESULTS: During the first 24 hours of incubation, the mean (+/- SE) rate of fluid secretion in nine cysts containing natural cyst fluid was 20.8 +/- 5.6 microliters per square centimeter of surface area per 24 hours, as compared with 2.3 +/- 3.6 microliters per square centimeter per 24 hours in nine cysts containing incubation medium. Each group of cysts was then incubated with forskolin, a nonspecific stimulator of adenylate cyclase activity, for an additional 24 hours. During this period the fluid-secretion rate of cysts containing natural cyst fluid did not change; however, the secretion rate of those containing incubation medium increased to 9.1 +/- 4.4 microliters per square centimeter per 24 hours (mean change, 6.8 +/- 1.1; P < 0.001). Cyst fluid stimulated fluid secretion by polarized monolayers of canine- and human-kidney cells. CONCLUSIONS: Renal cysts from patients with autosomal dominant polycystic kidney disease can secrete fluid, and net fluid secretion can be increased by unidentified secretagogues in the cyst fluid. These results suggest that the process of cyst enlargement may be susceptible to pharmacologic intervention.

Cells, Cultured↗
PubMed1986

Adrenergic influence on gallbladder function in experimental cholecystitis.

In experimental cholecystitis a net secretion of fluid to the gallbladder lumen is seen in animals with morphological signs of acute inflammation. This fluid secretion, which increases the intraluminal pressure in the obstructed gallbladder, is suggested to be influenced by non-cholinergic intramural gallbladder nerves activated by prostaglandins. In the present study in vivo we show that this fluid secretion, measured by a perfusion technique, is markedly inhibited by electrical activation of the splanchnic nerves that contain adrenergic fibres to the gallbladder and by intravenous administration of an alpha 2-adrenergic agonist, demonstrating that this fluid secretion can be modulated by activation of alpha 2-adrenergic receptors. In patients with an obstructed gallbladder outlet, inhibition of this secretion may reduce gallbladder distension and thus relieve biliary pain. The results suggest that pharmacological activation of adrenergic mechanisms could be useful in the treatment of cholecystitis and biliary pain.

Adrenergic Fibers↗
PubMed2004

Submucosal gland dysfunction as a primary defect in cystic fibrosis.

It has been proposed that defective submucosal gland function in CF airways is a major determinant of CF airway disease. We tested the hypothesis that submucosal gland function is defective early in CF subjects with minimal clinical disease. Functional assays of gland fluid secretion rate and viscosity were performed on freshly obtained nasal biopsies from 6 CF subjects and 5 non-CF controls (age range 2-22 years). Secretions from individual submucosal glands were visualized by light/fluorescence microscopy after orienting and immobilizing biopsy specimens in a custom chamber. The viscosity of freshly secreted gland fluid after pilocarpine, measured by fluorescence recovery after photobleaching of microinjected FITC-dextran, was 4.9 +/- 0.2- vs. 2.2 +/- 0.2-fold greater than water viscosity in CF vs. non-CF specimens, respectively (SE, P<10(-4)). Gland fluid secretion rate in CF specimens, measured by video imaging (4.5+/-0.5 nL/min/gland, n=6), was 2.7-fold reduced compared to non-CF specimens (n=3, P<0.05). Quantitative histology revealed similar size and morphology of submucosal glands in CF and non-CF specimens. Our results suggest that defective airway submucosal gland function is an early, primary defect in CF. Therapies directed at normalizing gland fluid secretion early in CF may thus reduce lung disease.

Adolescent↗
PubMed2006

Molecular identification and physiological roles of parotid acinar cell maxi-K channels.

The physiological success of fluid-secreting tissues relies on a regulated interplay between Ca(2+)-activated Cl(-) and K(+) channels. Parotid acinar cells express two types of Ca(2+)-activated K(+) channels: intermediate conductance IK1 channels and maxi-K channels. The IK1 channel is encoded by the K(Ca)3.1 gene, and the K(Ca)1.1 gene is a likely candidate for the maxi-K channel. To confirm the genetic identity of the maxi-K channel and to probe its specific roles, we studied parotid glands in mice with the K(Ca)1.1 gene ablated. Parotid acinar cells from these animals lacked maxi-K channels, confirming their genetic identity. The stimulated parotid gland fluid secretion rate was normal, but the sodium and potassium content of the secreted fluid was altered. In addition, we found that the regulatory volume decrease in acinar cells was substantially impaired in K(Ca)1.1-null animals. We examined fluid secretion from animals with both K(+) channel genes deleted. The secretion rate was severely reduced, and the ion content of the secreted fluid was significantly changed. We measured the membrane potentials of acinar cells from wild-type mice and from animals with either or both K(+) channel genes ablated. They revealed that the observed functional effects on fluid secretion reflected alterations in cell membrane voltage. Our findings show that the maxi-K channels are critical for the regulatory volume decrease in these cells and that they play an important role in the sodium uptake and potassium secretion process in the ducts of these fluid-secreting salivary glands.

Animals↗
PubMed1980

Relationship between renal fluid and Mg secretion in a glomerular marine teleost.

Renal tubular fluid secretion has been studied in seawater-acclimated winter flounder, Pseudopleuronectes americanus. Although this animal has a filtration kidney and a relatively high glomerular filtration rate (GFR = 1.35 ml . kg-1 . h-1), apparently more than half of the final urine volume was secreted fluid, and net fluid secretion was frequently observed. The dominant divalent ion excreted in the urine was Mg, of which 98% was secreted. A strong correlation (r = 0.98) was seen between secreted Mg and the rate of tubular fluid secretion. The calculated concentration of Mg in secreted fluid was 169 mM, a figure that was substantiated by values obtained for urine Mg concentration when urine flow was due almost entirely to tubular fluid secretion. Alterations in urine flow rate reflected changes in the rate of Mg secretion; however, no correlation was seen between GFR and secreted Mg, which may indicate independence of renal portal blood flow and glomerular blood flow. No relationship between Mg secretion and sodium reabsorption was apparent. These observations support the hypothesis that Mg secretion together with accompanying anions (Cl and SO4) accounts entirely for tubular fluid secretion in the winter flounder.

Animals↗
PubMed2006

Pharmacological characterization of the ergot alkaloid receptor in the salivary gland of the ixodid tick Amblyomma hebraeum.

Female ticks of the family Ixodidae osmoregulate by secreting the excess fluid of the blood meal back into the host's circulation via the salivary glands. At least three receptors control salivary fluid secretion in the tick Amblyomma hebraeum: (1) dopamine (DA) stimulates fluid secretion via a DA receptor, (2) ergot alkaloids (ErAs) stimulate fluid secretion via an ErA-sensitive receptor (the natural ligand of which has not been identified), and (3) a GABA receptor potentiates the action of DA and ErAs. Here we present some pharmacological properties of the ErA-sensitive receptor. Of the 11 ErAs we tested, (i) four were complete agonists (approximate concentration eliciting 50% maximum response is given in parentheses): dihydroergotamine (0.02 micromol l(-1)), ergonovine (ErN; 0.06 micromol l(-1)), methylergonovine (0.1 micromol l(-1)) and alpha-ergocriptine (0.9 micromol l(-1)); (ii) three were ;incomplete agonists' (approximate concentration eliciting 20% maximum response is given in parentheses): ergocorninine (3.5 micromol l(-1)), ergocristinine (7.5 micromol l(-1)) and ergocristine (10 micromol l(-1)); (C) three were partial agonists (approximate concentration eliciting the respective maximum response in parentheses): ergocornine (50% maximum by 1 micromol l(-1)), methysergide (28% maximum by 10 micromol l(-1)) and bromocriptine (22% maximum by 10 micromol l(-1)); and (D) one had no activity up to 1 mmol l(-1): ergothioneine. Bromocriptine and methysergide did not antagonize the action of DA, but were effective competitive antagonists of ErN, with K(i)s of approximately 0.3 micromol l(-1) and 11 micromol l(-1), respectively. Ergothioneine was not an antagonist at either the DA- or ErA-sensitive receptor. The putative protein kinase C activators, 1-oleoyl-2-acetyl-sn-glycerol (OAG) and 1,2-dioctanoyl-sn-glycerol (DiC8), neither stimulated salivary fluid secretion nor potentiated the action of DA or ErN. The putative protein kinase C inhibitors, bisindolymaleimide (BIM) and calphostin C did not inhibit the action of DA or ErN, although low concentrations of calphostin C (10 nmol l(-1)) appeared to potentiate the action of DA but not ErN. The ion transport inhibitors, furosemide and amiloride (both up to 1 mmol l(-1)), had no significant effect on DA-stimulated or ErN-stimulated fluid secretion.

Animals↗
PubMed1994

Secretion of plasminogen activators by cells cultured from subretinal fluid.

Secretion of plasminogen activators was examined in 11 cells cultures from subretinal fluid of patients with retinal detachment. The plasminogen activator production was compared to 4 retinal pigment epithelial cell cultures from post-mortem donors with no known retinal pathology. Plasminogen activator activity was evaluated by zymography and was corrected for the total cell protein in the cultures. Cells from subretinal fluid had more proteolytic activity and secreted more active urokinase-type plasminogen activator than retinal pigment epithelial cells of donor origin. It is possible that cells from subretinal fluid are modulated by the conditions in subretinal fluid to secrete more urokinase-type plasminogen activator, generally considered to be a sign of invasive growth or that the subretinal fluid cultures contain other cell types than solely retinal pigment epithelial cells, such as pigmented macrophages, with an active plasminogen activator production. Alternatively, retinal pigment epithelial cells detached into the subretinal fluid may represent a selected population of retinal pigment epithelial cells with a more active extracellular proteolysis.

Adolescent↗
PubMed1995

Effects of vasoactive intestinal peptide and its homologues on the acetylcholine-mediated secretion of fluid and protein from the rat submandibular gland.

1. Acetylcholine-mediated (ACh-mediated) secretion of fluid and protein from rat submandibular glands was enhanced by intravenous injection of vasoactive intestinal peptide (VIP) and of secretin but not of peptide histidine isoleucine (PHI) or gastric inhibitory peptide (GIP). 2. When VIP and ACh were administered together, the enhancement of fluid secretion was inhibited by pretreatment with atropine or 4-DAMP and the enhancement of protein secretion was inhibited by pretreatment with atropine or phentolamine. 3. The enhancement of the ACh-induced secretion of fluid by secretin was strongly inhibited by pretreatment with atropine, and it was weakly inhibited by pretreatment with phentolamine or haloperidol. 4. These results suggest that the synergistic effects of VIP, PHI, secretin and GIP on the ACh-mediated secretion of fluid and protein from the rat submandibular gland do not reflect the extent of the structural homology of each peptide to VIP.

Acetylcholine↗
PubMed2000

Effect of beta-antagonists on isoprenaline-induced secretion of fluid, amylase and protein by the parotid gland of the red kangaroo, Macropus rufus.

Selective and non-selective beta-adrenoceptor antagonists were used to block the increases in fluid, protein and amylase secretion caused by sympathomimetic stimulation of the parotid gland of red kangaroos during intracarotid infusion of isoprenaline. ICI118551 at antagonist/agonist ratios up to 300:1 caused increasing but incomplete blockade of fluid secretion, and protein/amylase release. Atenolol at antagonist/agonist ratios up to 300:1 was only marginally more potent than ICI118551 at blocking the fluid, protein and amylase responses. Propranolol at antagonist/agonist ratios of 30:1 was as effective at blocking fluid and protein secretion as the highest ratios of either atenolol or ICI118551. Simultaneous administration of atenolol (30:1) with ICI118551 (30:1) was not as potent as propranolol (30:1). Thus, the beta-adrenoceptor/s in the acini of the kangaroo parotid gland appear to have antagonist-binding affinities atypical of those found for eutherian tissues. The data are consistent with the gland possessing either a single anomalous beta-adrenoceptor or functional beta(2)-receptors in addition to the beta(1)-receptors which are characteristic of eutherian salivary glands.

Acetylcholine↗
PubMed1988

Effects of dobutamine and terbutaline on the secretion of glycoproteins from the acinar cells of the rat submandibular gland.

The actions of dobutamine (DOB) and terbutaline (TER) on the secretion of marker glycoprotein (GP) from the secretory cells of the glands and secretion of fluid from rat submandibular gland (SMG) were investigated in combination with two antagonists, metoprolol (MET) and ICI-118551 (ICI). The ED50 value of fluid secretion was 8.7 mg/kg for DOB and 5.9 mg/kg for TER. MET, administered prior to either agonists at a dose of 40 mg/kg, inhibited the fluid secretion. However, the blocking effects of ICI were considerably lower than those of MET. The electrophoretic profiles of GP in DOB-evoked saliva were similar to those in TER-evoked saliva, and included two characteristic main bands of GP I (130 KDa) and GP IV (21.5 KDa) from the acinar cells and a minor band of GP III (31 KDa) which originated in the cells of the granular tubules. When MET was administered at a dose of 5 mg/kg prior to DOB, the intensity of band I decreased, whereas that of band III did not change. These results showed that the SMG of rats contains both beta 1- and beta 2-adrenoceptors and that beta-receptors which mediate the secretion of GP from the acinus and fluid from the gland are mainly of the beta 1-subtype.

Adrenergic beta-Antagonists↗
PubMed1989

Patterns of pancreatic secretion in the anaesthetised guinea pig following stimulation with secretin, cholecystokinin octapeptide, or bombesin.

The guinea pig is frequently used for studies of the cellular mechanisms of pancreatic secretion. Despite this, little is known about the control of pancreatic secretion in this species. To remedy this omission, we have studied the effects of secretin, cholecystokinin (CCK) octapeptide, and bombesin on the secretion of fluid, electrolytes, and amylase in the anaesthetised guinea pig. While the actions of secretin were similar to those in other species, the actions of CCK were not. As well as stimulating amylase release, CCK evoked a marked fluid secretion whose electrolyte composition differed little from that evoked by secretin. Bombesin had actions similar to those of CCK. It is suggested that this fluid secretion is derived from pancreatic acini. Whether a similar secretory component exists in other species (including humans), albeit as a minor component, needs to be determined.

Amylases↗
PubMed1993

Duodenal mucosal alkaline secretion, permeability, and blood flow.

The relationship between duodenal mucosal alkaline secretion, permeability, and blood flow was examined in anesthetized rats. Duodenum was perfused with saline, and rate of luminal alkalinization (LA), mucosal permeability (clearance of 51Cr-EDTA from blood to lumen), effluent volume, mean arterial blood pressure (MABP), and blood flow (laser-Doppler flowmetry) were determined. Infusion of vasoactive intestinal polypeptide (VIP, 13.5 micrograms.kg-1 x h-1 i.v.) increased LA and fluid secretion but decreased MABP and mucosal permeability. The concentration of base in the secreted fluid was 45 mM. Systemic infusion of VIP (2.5 micrograms.kg-1 x h-1) increased LA and fluid secretion; the HCO3- concentration in secreted fluid was 86 mM. The lower VIP dose affected neither blood flow nor mucosal permeability. Both intravenous (10 mg/kg + 3 mg.kg-1 x h-1) and intraluminal (3 x 10(-3) M) N omega-nitro-L-arginine (L-NNA) increased LA and effluent volume; the HCO3- concentration in the secreted fluid was 38 and 44 mM, respectively. Intravenous, but not intraluminal, L-NNA increased mucosal permeability and decreased blood flow. Reduction of arterial blood pressure by blood withdrawal or by injection of prazosin (50 micrograms/kg i.v.) or hexamethonium (20 mg/kg i.v.) decreased LA and mucosal permeability. Prazosin decreased blood flow, whereas hexamethonium slightly increased blood flow. We conclude that NO may be an inhibitory regulator of LA and that both L-NNA and VIP increase LA via stimulation of active HCO3- transport. VIP probably increases HCO3- and fluid secretion by two separate ion transport mechanisms. No causal relationship exists between LA and blood flow, between LA and mucosal permeability, or between mucosal permeability and blood flow. A positive linear correlation exists between MABP and mucosal permeability, suggesting that marked changes of MABP may influence permeation of small water-soluble solutes across duodenal mucosa.

Animals↗
PubMed1980

The reflexion coefficient as a measure of transepithelial permeability in the isolated rabbit pancreas.

1. The reflexion coefficients of a number of non-electrolytes and electrolytes have been determined in the isolated rabbit pancreas. 2. The reflexion coefficients of the following non-electrolytes were: urea, -0.02; glycerol, 0.06; erythritol, 0.11; sorbitol, 0.41; mannitol, 0.42; arabinose, 0.72; xylose, 0.74, assuming a value of 1.00 for sucrose. 3. These values are equal within the experimental error to values previously obtained with a tracer technique for the same preparation, but they are significantly lower than those reported by other investigators for the isolated perfused cat pancreas. 4. Addition of 100 mM-sucrose to the bathing medium resulted in proportionally increased Na+ and K+ concentrations in the secreted fluid. The secreted fluid remained isotonic with the bathing medium under all circumstances. 5. Addition of 10(-5) M-carbachol to the bathing medium led to a reduction in the reflexion coefficient of sucrose from 1 to 0.85, but only when 25 mM-sucrose was used. 6. The reflexion coefficients of electrolytes were: NaCl, 0.50; KCl, 0.51; NaHCO3, 0.52 and choline chloride, 1.02. 7. It is concluded that the isolated rabbit pancreas is highly permeable, both to electrolytes and to small non-electrolytes, probably being more leaky than any other epithelium studied so far.

Animals↗
PubMed1977

Effects of long chain fatty acids on solute absorption: perfusion studies in the human jejunum.

Perfusion studies were performed in healthy volunteers to test the hypothesis that net fluid secretion induced by fatty acids is accompanied by parallel reduction in solute transport. Ricinoleic acid provoked a marked net secretion of fluid and concomitantly inhibited the absorption of all solutes tested; these included glucose, xylose, L-leucine, L-lysine, Folic acid, and 2-mono-olein. Oleic acid also reduced net fluid and solute transport, but was less potent in reducing solute absorption than was ricinoleic acid. When fluid secretion was induced osmotically with mannitol, glucose and xylose absorption was not affected. The mechanism for this generalised effect of fatty acids on solute absorption is uncertain, possibly nonspecific, and might be related to mucosal damage and altered mucosal permeability induced by these agents.

Betaine↗
PubMed2002

Ca(2+)-dependent stimulation of alveolar fluid clearance in near-term fetal guinea pigs.

We investigated the importance of changes in intracellular Ca(2+) concentration ([Ca(2+)](i)) for amiloride-sensitive alveolar fluid clearance (AFC) in late-gestational guinea pigs. Fetal guinea pigs of 61, 68, and 69 days (term) gestation were investigated under normal conditions and after oxytocin-induced preterm labor. AFC or alveolar fluid secretion was measured using an impermeable tracer technique. At 61 days gestation there was net secretion of fluid into the lungs, and at birth the lungs cleared 49 +/- 7% of the instilled fluid volume over 1 h. Induction of preterm labor with oxytocin induced AFC at 61 days gestation. When present, AFC was inhibited or reversed to net fluid secretion by amiloride (10(-3) M). Inhibition of membrane Ca(2+) channels by verapamil (10(-4) M) or depletion of intracellular Ca(2+) by thapsigargin (10(-5) M) reduced AFC when net AFC was evident. Amiloride lacked an inhibitory effect on AFC when instilled with verapamil or thapsigargin. The results indicate that AFC via amiloride-sensitive pathways develops during late gestation, and that inducing preterm labor precociously may activate such pathways. Our results suggest that Ca(2+) may act as a second messenger in mediating catecholamine-stimulated AFC.

Amiloride↗
PubMed1980

Parotid secretion of fluid and amylase in rabbits during feeding.

Saliva has been collected from conscious rabbits in response to feeding pellets and carrots and amylase concentrations and flow-rates were measured. Saliva was collected from a polythene tube permanently inserted into the main duct, which, in most cases, kept patent for about a fortnight without any obvious decrease in the secretory capacity of the glands. 2. With pellets the flow-rate varied between 50 and 1250 microliter./min, and the corresponding amylase concentration was relatively constant around 250 units/ml. When carrots were fed, the flow-rates were about threefold lower, but the amylase concentration was raised to a mean value around 1000 units/ml. In spite of the differences in flow-rates, the two kinds of food promoted the same maximum output of amylase, and the output for both kinds of food promoted the same maximum output of amylase, and the output for both kinds of food was found to increase with the flow-rate. 3. The amylase concentration in the saliva decreased after pre- or post-ganglionic sympathetic denervation, reducing the output of amylase by about 50%. However, the amylase concentration was further lowered by beta-adrenoceptor block, which decreased the output by an additional 25%, suggesting that circulating catecholamines contributed to the secretion of amylase. 4. The fluid secretion in response to pellets and carrots was mainly dependent on parasympathetic activity, and for both kinds of food the range of flow-rates was unaltered by sympathectomy or beta-adrenoceptor block. However, at flow-rates below 50 microliter./min, where 25% of all samples with carrots were obtained, sympathetic activity may have contributed significantly to the fluid secretion. 5. In experiments on anaesthetized rabbits, frequency-response curves for amylase and fluid secretion in response to parasympathetic and sympathetic activation were obtained. A comparison between these observations and those obtained in the conscious animals during feeding suggests a parasympathetic activity mainly between 1 and 5 Hz and a sympathetic around 1 Hz. 6. It is concluded that both parasympathetic and sympathetic secretory nerves are reflexly activated during feeding, and that the normal secretion during a meal is dependent on an interplay between the nerves. The results suggest that at least two different afferent nervous pathways are involved in the control of the secretory nerves.

Amylases↗