HCO3 Secretion Research Articles

Rabbit Cholera: Inhibitory Effect of Tenuazonic Acid on Cholera-Induced Secretion of Water and Electrolytes

The effect of tenuazonic acid, an inhibitor of protein synthesis, on cholera-induced secretion was studied in rabbit jejunum in vivo. Tenuazonic acid inhibited significantly net water and ion secretion induced by cholera toxin. The over-all inhibition of net ion flux was 72%; of the total reduction in net anion flux, 57% was due to a decrease in Cl and 43% to a decrease in HCO3. The drug had no significant effect on the net absorption of H2O, Na, Cl, and K, or net secretion of HCO3 in jejunal loops not incubated with purified cholera toxin, nor did it alter the linear relationship between net fluxes of Na and H2O observed during absorption or secretion. It is suggested that the effect of tenuazonic acid may be directed toward either the cell membrane or enzymes.

Rabbit Cholera: Effects of Cycloheximide on Net Water and Ion Fluxes and Transmural Electric Potentials

Effects of cycloheximide on net H2O and electrolyte fluxes and transmural electric potentials were studied in vivo in paired loops of rabbit jejunum randomly incubated with either cholera toxin or control peptone broth. Untreated animals showed a profound secretion of H2O, Na, and HCO3, and slight secretion of Cl in response to cholera when compared with paired control loops. Pretreatment with cycloheximide abolished secretion of H2O and Cl in response to cholera, and greatly reduced Na and HCO3 secretion. Over-all reduction in net ion flux was about 75%; inhibition of anion secretion was about equal for Cl and HCO3. Potassium absorption was significantly decreased in both control and cholera segments in pretreated animals when compared with untreated controls. Transmural electric potentials did not reflect either the direction or magnitude of net H2O or ion fluxes. It is concluded that: (1) pretreatment with cycloheximide effectively blocks the response to cholera toxin; (2) potassium absorption is decreased in pretreated animals, otherwise the drug has no significant effects on net water or ion fluxes in control segments; (3) the drug has effects on transmural potentials unrelated to the severity of the cholera response; and (4) drug effects on net anion fluxes are about equal for Cl and HCO3.

Evidence for Na-H Exchange in the Rabbit Pancreas

WE have found that pancreatic juice secretion can be maintained at a high rate even when all exogenous HCO3 is replaced by another weak acid anion such as acetate. When acetate is secreted by the rabbit pancreas in vitro, juice flows at rates of 30–90% of control1 and acetate reaches a concentration up to three times that in the ambient bathing solution. HCO3 is not essential for juice production and so these data suggest that active transport of H or OH ions is responsible for normal HCO3 secretion. We have therefore examined the effect of alterations of ambient pH on cell pH. Our data indicate the existence of an Na-H exchange mechanism at the serosal (bath-facing) membrane.

The effect of a sympatho- and a parasympathomimetic drug on the electrolyte concentrations of primary and final saliva of the rat submaxillary gland.

Salivary glands are generally supposed to produce their secretions in 2 stages: 1. A plasma-like secretion is formed in the acinar-intercalated duct region of the gland, the rate of production but not the electrolyte composition of this fluid being increased by gland stimulation. 2. This primary saliva is then modified during its passage along the gland duct system by processes of Na reabsorption and K and HCO3 secretion.

Electrolyte concentrations in primary and final saliva of the rat sublingual gland studied by micropuncture and catheterization techniques.

The salivary electrolyte concentrations at various secretory rates have been studied in the rat sublingual gland and compared with the concentrations found in acinar-intercalated duct (primary) fluid obtained by micropuncture. The primary fluid had the following composition: [Na]=126±1.6 (S.E.M.,n=39) mEq/l; [K]=11.9±1.2 mEq/l (n=39); [Cl]=99.3±2.3 mEq/l (n=33). The Na and K concentrations differed significantly from those of plasma and from those observed previously in the primary fluid of rat parotid and submaxillary glands. The composition of primary fluid was not altered by carbachol stimulation. After carbachol stimulation, the final saliva, like that of the human but unlike that of the cat and dog sublingual gland, was hypotonic and the electrolyte concentrations showed flow-rate dependence. At the lowest flow rate the Na concentrations averaged 24.6±3.9 mEq/l (n=25) which fell first to a minimum and then rose to a plateau of about 60 mEq/l as flow rate increased to a maximum. The excretory curve showed no tendency to approach the concentrations seen in primary saliva. The K excretory curve was typical of that seen in most other salivary glands, having high concentrations at low flow rates which fell towards a plateau above primary fluid levels as flow rate increased. The salivary bicarbonate concentration was always above that in plasma; it tended to rise to a plateau of about 48 mEq/l at the highest flow rates. This concentration is probably greater than that present in primary fluid although the primary levels have not been measured directly. The results are best interpreted in terms of a modified two-stage hypothesis. First a primary, Na-rich, K-poor secretion is formed in the acinar-intercalated duct region whose composition, although decidedly not plasma-like, is constant irrespective of the degree of gland stimulation. Then, secondarily, this fluid is modified during passage along the striated and excretory ducts by processes of Na reabsorption and K and HCO3 secretion. These secondary transport processes are not transport-maximum-limited but appear to increase with increasing degree of stimulation resulting in a phenomenon which could be termed acinar-tubular balance. Although it has not proven possible to micropuncture striated ducts in the rat submaxillary or parotid glands, in the sublingual gland we were able to do so in a few cases. For the first time we are able to offer direct proof that these ducts do contain hypotonic fluid.

Effects of acetazolamide and acid-base changes on biliary and pancreatic secretion.

ARTICLESEffects of acetazolamide and acid-base changes on biliary and pancreatic secretionBH Pak, SS Hong, HK Pak, and SK HongBH Pak, SS Hong, HK Pak, and SK HongPublished Online:01 Mar 1966https://doi.org/10.1152/ajplegacy.1966.210.3.624MoreSectionsPDF (921 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByHepatobiliary acid-base homeostasis: Insights from analogous secretory epitheliaJournal of Hepatology, Vol. 74, No. 2Molecular Mechanism of Pancreatic and Salivary Gland Fluid and HCO3− SecretionMin Goo Lee, Ehud Ohana, Hyun Woo Park, Dongki Yang, and Shmuel Muallem1 January 2012 | Physiological Reviews, Vol. 92, No. 1Cell Physiology of Pancreatic DuctsMECHANISMS OF BICARBONATE SECRETION IN THE PANCREATIC DUCTAnnual Review of Physiology, Vol. 67, No. 1Expression and distribution of the Na+-HCO3− cotransporter in human pancreasChristopher R. Marino, Virginia Jeanes, Walter F. Boron, and Bernhard M. Schmitt1 August 1999 | American Journal of Physiology-Gastrointestinal and Liver Physiology, Vol. 277, No. 2INHIBITORY EFFECT OF OUABAIN AND ACETAZOLAMIDE ON SECRETIN-STIMULATED PANCREATIC EXOCRINE SECRETION IN ANAESTHETIZED DOGClinical and Experimental Pharmacology and Physiology, Vol. 16, No. 3Effects of Inhibition of Angiotensin Converting Enzyme and Carbonic Anhydrase on Fluid Production by Ciliary Process, Choroid Plexus, and PancreasJournal of Ocular Pharmacology and Therapeutics, Vol. 5, No. 4Importance of carbonic anhydrase for canalicular and ductular choleresis in the pigActa Physiologica Scandinavica, Vol. 133, No. 4DCCD ( N, N ′-Dicyclohexylcarbodiimide) Inhibits Biliary Secretion of HCO 38 July 2009 | Scandinavian Journal of Gastroenterology, Vol. 22, No. 2Mechanism of hepatic bicarbonate secretion and bile acid independent bile secretionEuropean Journal of Clinical Investigation, Vol. 13, No. 3Abolished relationship between pancreatic HCO -3 secretion and arterial pH during carbonic anhydrase inhibitionActa Physiologica Scandinavica, Vol. 114, No. 1Pancreatic basal secretion in alcohol-fed and normal dogsDigestive Diseases and Sciences, Vol. 26, No. 9Relationship between plasma pH and pancreatic HCO 3- secretion at different intravenous secretin infusion ratesActa Physiologica Scandinavica, Vol. 109, No. 2Die Besonderheiten des N-Stoffwechsels und die Produktivität der Tiere in Abhängigkeit von der Konzentration des HCO 3- , und CO 2 in den Geweben25 September 2009 | Archiv für Tierernaehrung, Vol. 30, No. 1-3Respiratory exchanges and acid-base balance during perfusion ofex vivo isolated pancreasThe American Journal of Digestive Diseases, Vol. 21, No. 5The secretion of electrolytes by the pancreasThe American Journal of Clinical Nutrition, Vol. 26, No. 3Bile SecretionClinics in Gastroenterology, Vol. 2, No. 1Lipid soluble weak organic acid buffers as ?substrate? for pancreatic secretionPfl�gers Archiv European Journal of Physiology, Vol. 323, No. 2Influence of bicarbonate-CO2- and glycodiazine buffer on the secretion of the isolated cat's pancreasPfl�gers Archiv European Journal of Physiology, Vol. 329, No. 4An Assessment of Models for Pancreatic SecretionGastroenterology, Vol. 59, No. 6Effect of Secretin and Acetazolamide on the Volume and Electrolyte Composition of Hepatic Bile in ManGastroenterology, Vol. 56, No. 2The additive effect of acetazolamide and ouabain on pancreatic secretion in vitroPfl�gers Archiv European Journal of Physiology, Vol. 311, No. 3The source of duodenal aspirate in man.Gut, Vol. 9, No. 4The Ins and Outs of Bicarbonate in the Alimentary TractGastroenterology, Vol. 54, No. 4Response to Secretin in ManGastroenterology, Vol. 54, No. 2 More from this issue > Volume 210Issue 3March 1966Pages 624-628 Copyright & PermissionsCopyright © 1966 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1966.210.3.624PubMed5933216History Published online 1 March 1966 Published in print 1 March 1966 Metrics

Effect of d-1-ethionine on electrolyte secretion of the dog pancreas

The secretion of fluid and electrolytes, as well as amylase, was studied in response to secretin and pancreozymin stimulation in unanesthetized dogs fitted with a Thomas-type duodenal fistula by inserting a cannula directly into the main pancreatic duct before and during a 3-week period of ethionine administration. In addition to the well-established destructive effect of d-l-ethionine on the acinar cell and its secretion of enzymes, changes occurred in the secretion of HCO3 and H2O in response to secretin. During the early phase of ethionine intoxication (weeks 1–2) HCO3 concentration fell despite preservation of the volume rate of flow. During the second and third weeks, HCO3 concentration was preserved despite marked reduction in volume rate of flow. It is suggested that these findings may be correlated with changes in ductular as well as acinar cells. Na and K concentration, juice osmolality, and the reciprocal Cl-HCO3 relationship were unaltered.