Effects of acetazolamide and metabolic acidosis and alkalosis upon gastric acid secretion

1962 ◽  
Vol 202 (3) ◽  
pp. 429-436 ◽  
Author(s):  
Frank M. Byers ◽  
Paul H. Jordan ◽  
Thomas H. Maren
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Acid Secretion ◽  
Metabolic Alkalosis ◽  
Suppressive Effect ◽  
Low Doses ◽  
Heidenhain Pouch ◽  
Feeding Experiments ◽  
Initial Reduction ◽  
Higher Doses

The gastric H+ secretory responses to i.v. HCl, NaHCO3, and acetazolamide were studied in Heidenhain-pouch dogs that had been stimulated to secrete by feeding. Acetazolamide in low doses (5 mg/kg) gave a 65% reduction in H+ output for 2–4 hr, after which H+ secretion increased above normal, coincident with renal HCO3– loss and metabolic acidosis. Higher doses produced a greater systemic acidosis and resulted in less initial reduction of H+ and greater augmentation. Doses of 75–100 mg/kg, given 17 hr before feeding to produce a systemic acidosis, resulted in increased secretion, even though sufficient drug remained in the plasma to inhibit tissue carbonic anhydrase. Metabolic acidosis (i.v. HCl) initially suppressed but later augmented gastric H+. Acetazolamide had no suppressive effect in the presence of either an HCl- or acetazolamide-induced acidosis. Metabolic alkalosis (i.v. NaHCO3) reduced gastric H+ in regular feeding experiments and in dogs made acidotic by acetazolamide.

Effects of bombesin on food intake and gastric acid secretion in cats

1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Fistula ◽  
Single Class ◽  
Heidenhain Pouch ◽  
Daily Food Intake ◽  
Feeding Experiments ◽  
Daily Food

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.

Effect of vagal innervation on acid and pepsin response to histamine and gastrin

1964 ◽  
Vol 206 (5) ◽  
pp. 1068-1076 ◽  
Author(s):  
Edward P. Passaro ◽  
Morton I. Grossman
Keyword(s):  
Acid Secretion ◽  
Low Doses ◽  
Pepsin Secretion ◽  
Heidenhain Pouch ◽  
Wide Range ◽  
Vagal Innervation ◽  
Sustained Increase

The acid and pepsin responses to a wide range of doses of gastrin extract and of histamine were determined in dogs that had both a fistula of the vagally innervated main stomach (GF) and a vagally denervated Heidenhain pouch (HP). The GFs gave the same maximal acid response with gastrin as with histamine whereas the maximal acid response of the HPs to gastrin was only 45% of that to histamine. Opening the GF increased the response of the HP to submaximal doses of gastrin and, to a lesser extent, of histamine. With the GF open, peak rates of secretion from the HP were not sustained, particularly with gastrin stimulation. Sustained increase in pepsin output over basal levels occurred in GFs with very low doses of gastrin but not with any dose of histamine and in HPs with all doses of histamine and of gastrin tested. In both GFs and HPs doses of histamine that were supramaximal for acid secretion suppressed pepsin secretion without a concomitant fall in acid secretion, a phenomenon not seen with stimulation with gastrin.

Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis

1976 ◽  
Vol 40 (4) ◽  
pp. 559-567 ◽  
Author(s):  
F. M. Hasan ◽  
H. Kazemi
Keyword(s):  
Metabolic Acidosis ◽  
Carbonic Anhydrase ◽  
Metabolic Alkalosis ◽  
Control Mechanism ◽  
Respiratory Acidosis ◽  
Experimental Conditions ◽  
Relative Contribution ◽  
Intraventricular Injections ◽  
Anesthetized Dogs ◽  
The Brain

Regulation of CSF HCO3-in respiratory acidosis was studied in light of the “dual contribution theory,” which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504–512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.

Involvement of 5-Hydroxytryptamine in Platelet Aggregation In Vivo in Rats and Guinea Pigs

1989 ◽  
Vol 61 (03) ◽  
pp. 463-467 ◽  
Author(s):  
G M Smith
Keyword(s):  
Platelet Count ◽  
Guinea Pigs ◽  
Platelet Adhesion ◽  
Adenosine Diphosphate ◽  
Rate Of Return ◽  
Low Doses ◽  
Dose Dependent ◽  
Higher Doses ◽  
Rat Platelets

SummaryIn this study, 5-hydroxytryptamine (5-HT) caused a dose- dependent fall in the circulating platelet count suggesting that 5-HT receptors are activated in rat platelets to cause platelet adhesion and aggregation. When low doses of adenosine diphosphate (ADP) were simultaneously injected with 5-HT, there was a significant potentiation of the responses to ADR Ketanserin significantly reduced the potentiated responses. When higher doses of ADP were infused with bolus injections of 5-HT there was no potentiation and ketanserin did not reduce these responses. Ketanserin did not inhibit the collagen-induced fall in circulating platelet count, but did significantly increase the rate of return to the basal platelet count compared with control. 5-HT did not cause a fall in platelet count in guinea-pigs

Induction of renal phosphoenolpyruvate carboxykinase mRNA: suppressive effect of glucose

1989 ◽  
Vol 257 (1) ◽  
pp. F145-F151
Author(s):  
A. S. Pollock
Keyword(s):  
Metabolic Acidosis ◽  
Phosphoenolpyruvate Carboxykinase ◽  
Suppressive Effect ◽  
Oral Glucose ◽  
Prolonged Fasting ◽  
Glucose Loading ◽  
Glucose Administration ◽  
Liver And Kidney ◽  
Gluconeogenic Enzyme ◽  
Effect Of Glucose

The mRNA for the important gluconeogenic enzyme phosphoenolpyruvate carboxykinase (GTP) (PEPCK; EC 4.1.1.32) is expressed in liver and kidney. In the kidney, acidosis is a unique and potent stimulus, whereas insulin, the major counterregulatory hormone of gluconeogenesis, has no effect. In this study, we find that oral glucose administration to rats rapidly decreases the abundance of renal PEPCK mRNA by 50–72%. This reduction takes place in normal euglycemic, in insulin-induced hypoglycemic, and in streptozotocin-induced hyperglycemic diabetic animals. The effect of glucose is not seen in the presence of metabolic acidosis, whether induced by NH4Cl or by prolonged fasting. Therefore, it appears that oral glucose loading is a physiological suppressor of renal PEPCK message abundance, although not in acidosis.

Effect of insulin on free fatty acid uptake by hepatocytes in the duck

1984 ◽  
Vol 102 (3) ◽  
pp. 381-386 ◽  
Author(s):  
R. Gross ◽  
P. Mialhe
Keyword(s):  
Fatty Acids ◽  
Growth Hormone ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Free Fatty Acids ◽  
Fatty Acid Uptake ◽  
Acid Uptake ◽  
Low Doses ◽  
Higher Doses

ABSTRACT To elucidate the hypolipacidaemic effect of insulin in ducks, its action on the uptake of free fatty acids (FFA) by duck hepatocytes was determined. At low doses (10 mu./l) insulin stimulated FFA uptake. This effect was not observed with higher doses of insulin (20, 30 and 50 mu./l). Growth hormone at physiological concentrations and corticosterone (14·4 nmol/l) decreased basal activity, probably by reducing glucose metabolism and consequently α-glycerophosphate (α-GP) supply. Insulin was able to reverse the inhibition induced by GH and corticosterone on both FFA uptake and α-GP production. These results therefore suggest that the hypolipacidaemic effect of insulin may be partly mediated by its action on hepatic FFA uptake. J. Endocr. (1984) 102, 381–386

Regulation of ion transport by pH and [HCO3−] in isolated gills of the crab Neohelice (Chasmagnathus) granulata

2008 ◽  
Vol 294 (3) ◽  
pp. R1033-R1043 ◽  
Author(s):  
Martin Tresguerres ◽  
Scott K. Parks ◽  
Sebastian E. Sabatini ◽  
Greg G. Goss ◽  
Carlos M. Luquet
Keyword(s):  
Carbonic Anhydrase ◽  
Ion Transport ◽  
Acid Secretion ◽  
Cellular Response ◽  
Low Ph ◽  
Potential Difference ◽  
Anion Exchangers ◽  
Transepithelial Potential Difference ◽  
Chasmagnathus Granulata ◽  
First Time

Posterior isolated gills of Neohelice ( Chasmagnathus) granulatus were symmetrically perfused with hemolymph-like saline of varying [HCO3−] and pH. Elevating [HCO3−] in the saline from 2.5 to 12.5 mmol/l (pH 7.75 in both cases) induced a significant increase in the transepithelial potential difference ( Vte), a measure of ion transport. The elevation in [HCO3−] also induced a switch from acid secretion (−43.7 ± 22.5 μequiv·kg−1·h−1) in controls to base secretion (84.7 ± 14.4 μequiv·kg−1·h−1). The HCO3−-induced Vte increase was inhibited by basolateral acetazolamide (200 μmol/l), amiloride (1 mmol/l), and ouabain (5 mmol/l) but not by bafilomycin (100 nmol/l). The Vte response to HCO3− did not take place in Cl−-free conditions; however, it was unaffected by apical SITS (2 mmol/l) or DIDS (1 mmol/l). A decrease in pH from 7.75 to 7.45 pH units in the perfusate also induced a significant increase in Vte, which was matched by a net increase in acid secretion of 67.8 ± 18.4 μequiv kg−1 h−1. This stimulation was sensitive to basolateral acetazolamide, bafilomycin, DIDS, and Na+-free conditions, but it still took place in Cl−-free saline. Therefore, the cellular response to low pH is different from the HCO3−-stimulated response. We also report V-H+-ATPase- and Na+-K+-ATPase-like immunoreactivity in gill sections for the first time in this crab. Our results suggest that carbonic anhydrase (CA), basolateral Na+/H+ exchangers and Na+-K+-ATPase and apical anion exchangers participate in the HCO3−-stimulated response, while CA, apical V-H+-ATPase and basolateral HCO3−-dependent cotransporters mediate the response to low pH.

scholarly journals An ontogenic study of receptor mechanisms by which acute administration of low-doses of methamphetamine suppresses DOI-induced 5-HT2A-receptor mediated head-twitch response in mice

2022 ◽  
Vol 23 (1) ◽  
Author(s):  
Yina Sun ◽  
Seetha Chebolu ◽  
Denise Henry ◽  
Sandeep Lankireddy ◽  
Nissar A. Darmani
Keyword(s):  
Suppressive Effect ◽  
Inhibitory Effect ◽  
Acute Administration ◽  
Low Doses ◽  
Head Twitch ◽  
Twitch Response ◽  
Way 100635 ◽  
Direct Acting ◽  
Head Twitch Response ◽  
Stimulation Of

Abstract Background Methamphetamine (MA) is a non-selective monoamine releaser and thus releases serotonin (5-HT), norepinephrine (NE) and dopamine (DA) from corresponding nerve terminals into synapses. DOI ((±)-2, 5-dimethoxy-4-iodoamphetamine) is a direct-acting serotonergic 5-HT2A/C receptor agonist and induces the head-twitch response (HTR) via stimulation of 5-HT2A receptor in mice. While more selective serotonin releasers such as d-fenfluramine evoke the HTR, monoamine reuptake blockers (e.g., cocaine) suppress the DOI-evoked HTR via indirect stimulation of serotonergic 5-HT1A- and adrenergic ɑ2-receptors. Since the induction of HTR by DOI is age-dependent, we investigated whether: (1) during development MA can evoke the HTR by itself, and (2) acute pretreatment with either the selective 5-HT2A receptor antagonist EMD 281014 or low-doses of MA can: (i) modulate the DOI-induced HTR in mice across postnatal days 20, 30 and 60, and (ii) alter the DOI-induced c-fos expression in mice prefrontal cortex (PFC). To further explore the possible modulatory effect of MA on DOI-induced HTR, we investigated whether blockade of inhibitory serotonergic 5-HT1A- or adrenergic ɑ2-receptors by corresponding selective antagonists (WAY 100635 or RS 79948, respectively), can prevent the effect of MA on DOI-induced HTR during aging. Results Although neither EMD 281014 nor MA by themselves could evoke the HTR, acute pretreatment with either EMD 281014 (0.01, 0.05 and 0.1 mg/kg, i.p.) or MA (1, 2.5, 5 mg/kg, i.p.), dose-dependently suppressed the DOI-induced HTR across ages. While WAY 100635 significantly reversed the inhibitory effect of MA in 20- and 30-day old mice, RS 79948 failed to significantly counter MA’s inhibitory effect. Moreover, DOI significantly increased c-fos expressions in several PFC regions. EMD 281014 prevented the DOI-induced increases in c-fos expression. Despite the inhibitory effect of MA on DOI-induced HTR, MA alone or in combination with DOI, significantly increased c-fos expression in several regions of the PFC. Conclusion The suppressive effect of MA on the DOI-evoked HTR appears to be mainly due to functional interactions between the HTR-inducing 5-HT2A receptor and the inhibitory 5-HT1A receptor. The MA-induced increase in c-fos expression in different PFC regions may be due to MA-evoked increases in synaptic concentrations of 5-HT, NE and/or DA.

Effect of methacholine chloride on rheology and transport of canine tracheal mucus

1979 ◽  
Vol 47 (1) ◽  
pp. 26-31 ◽  
Author(s):  
M. King ◽  
N. Viires
Keyword(s):  
Mechanical Properties ◽  
Elastic Modulus ◽  
Base Line ◽  
Low Doses ◽  
Mucociliary Transport ◽  
Frog Palate ◽  
High Doses ◽  
Tracheal Mucus ◽  
Higher Doses ◽  
Cytology Brush

The effect of methacholine chloride (M) on tracheal mucus was investigated in three conscious tracheostomized dogs. Aerosols of M in concentrations of 2--32 mg/ml were delivered intratracheally for 1 min. Mucus was sampled with a cytology brush at 2 min postchallenge and at irregular intervals thereafter. The mechanical properties of each sample were determined in the magnetic microrheometer, and correlated with mucociliary transportability as assayed by the frog palate technique. With high doses of M, there was an increase in volume of secretion collected per unit time. The elastic modulus (G′) at 2 min postchallenge went up (to 1.5 x 2.3 x control for 16 and 32 mg/ml, respectively) then fell below control before returning to base line after 30 or 45 min. With low doses of M (2--8 mg/ml) the secretion rate was also above control, but only a decrease in G′ (to 0.54 x control) was observed. The decrease in G′ at low doses did not significantly alter the frog palate transport rate; however, the increase at higher doses did impede mucociliary transport.

Acid secretion in isolated guinea pig colon

1987 ◽  
Vol 253 (2) ◽  
pp. G155-G164 ◽  
Author(s):  
Y. Suzuki ◽  
K. Kaneko
Keyword(s):  
Carbonic Anhydrase ◽  
Guinea Pig ◽  
Acid Secretion ◽  
Proximal Part ◽  
Bathing Solution ◽  
Maximal Effect ◽  
Dose Dependency ◽  
Ussing Chambers ◽  
Mucosal Acidification ◽  
Ph Stat

Isolated guinea pig distal colons secreted acid into the mucosal bathing solution at a rate of 1.0-1.5 mumol X cm-2 X h-1 when the preparations were mounted in Ussing chambers and bathed with HCO3(-)-CO2-free solution. The rates of the acidification and alkalinization of the solutions were measured by a pH stat system or calculated from changes in the pH of the solution. The acid secretion was localized in the middle and distal parts of the colon but absent in the proximal part of the colon and the cecum. The mucosal acidification was accompanied by serosal alkalinization, the rate of the latter being approximately 60% of the former. A carbonic anhydrase inhibitor, methazolamide (10(-4) M), reduced both the mucosal acidification and serosal alkalinization rates by a similar magnitude. The mucosal acidification was completely abolished by mucosal K+-free conditions but unaffected by mucosal Na+-free conditions. Ouabain added to the mucosal solution promptly inhibited the acid secretion. Dose dependency of the inhibition conformed to the Michaelis-Menten equation with a half-maximal effect at 4 X 10(-6) M. When the pH of the mucosal solution was reduced to 4.3, the rate of the mucosal acidification remained essentially the same as that at pH = 7.4. Vanadate (10(-4) M) added to both the mucosal and serosal solutions significantly reduced the mucosal acidification rate. These results suggest that CO2 derived from the epithelial metabolism is hydrated by carbonic anhydrase in the cell and released H+ enters the mucosal solution while HCO3- enters the serosal solution. H+ exit across the mucosal membrane may be mediated by H+-ATPase that is sensitive to ouabain.

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