Secretion In Gastric Mucosa Research Articles

HDAC6/HNF4\u03b1 loop mediated by miR-1 promotes bile acids-induced gastric intestinal metaplasia

BackgroundGastric intestinal metaplasia (IM) is considered a precancerous lesion, and bile acids (BA) play a critical role in the induction of IM. Ectopic expression of HNF4α was observed in a BA-induced IM cell model. However, the mechanisms underlying the upregulation of the protein in IM cells remains to be elucidated.MethodsThe effects of HNF4α on gastric mucosal cells in vivo were identified by a transgenic mouse model and RNA-seq was used to screen downstream targets of deoxycholic acid (DCA). The expression of pivotal molecules and miR-1 was detected by immunohistochemistry and in situ hybridization in normal, gastritis and IM tissue slides or microarrays. The transcriptional regulation of HDAC6 was investigated by chromatin immunoprecipitation (ChIP) and luciferase reporter assays.ResultsThe transgenic mouse model validated that HNF4α stimulated the HDAC6 expression and mucin secretion in gastric mucosa. Increased HDAC6 and HNF4α expression was also detected in the gastric IM cell model and patient specimens. HNF4α could bind to and activate HDAC6 promoter. In turn, HDAC6 enhanced the HNF4α protein level in GES-1 cells. Furthermore, miR-1 suppressed the expression of downstream intestinal markers by targeting HDAC6 and HNF4α.ConclusionsOur findings show that the HDAC6/HNF4α loop regulated by miR-1 plays a critical role in gastric IM. Blocking the activation of this loop could be a potential approach to preventing BA-induced gastric IM or even gastric cancer (GC).

Interaction of Constitutive Nitric Oxide Synthases with Cyclooxygenases in Regulation of Bicarbonate Secretion in the Gastric Mucosa.

Neuronal NO synthase blocker 7-nitroindazole suppressed bicarbonate secretion in rat gastric mucosa induced by mild local irritation with 1 M NaCl (pH 2.0). Non-selective blocker of neuronal and endothelial synthases, Nω-nitro-L-arginine (L-NNA), did not affect HCO3- production, but inhibited secretion after pretreatment with omeprazole. Non-selective cyclooxygenase blocker indomethacin inhibited HCO3- production under conditions of normal synthase activity and in the presence of L-NNA, but was ineffective when co-administered with 7-nitroindazole. It was concluded that neuronal and endothelial synthases are involved in different mechanisms of regulation of HCO3- secretion in the gastric mucosa induced by mild irritation. Activation of neuronal synthase stimulated HCO3- production, which is mediated mainly through activation of cyclooxygenase. Theoretically, activation of endothelial synthase should suppress HCO3- production. The effect of endothelial synthase depends on acid secretion in the stomach and bicarbonate concentration in the submucosa, as it was demonstrated in experiments with intravenous NaHCO3 infusion.

A C-Terminal Coiled-Coil Region of CagL is Responsible for Helicobacter Pylori-Induced Il-8 Expression.

Interleukin-8 (IL-8) is a potent neutrophil-activating chemokine which triggers the infiltration and migration of neutrophils into areas of bacterial infection. Helicobacter pylori-infected patient studies as well as animal models have revealed that H. pylori type I strains carrying an intact cytotoxin-associated gene pathogenicity island (cag-PAI) with a functional type IV secretion system (T4SS) induce IL-8 expression and secretion in gastric mucosa. This gastric mucosal IL-8 expression correlates with severe histological changes due to H. pylori infection.In the present study, we explored a new recognition pattern on the bacterial adhesion protein CagL inducing IL-8 expression in H. pylori-infected host cells. To analyze the secreted IL-8 concentration, we performed IL-8 enzyme-linked immunosorbent assay (ELISA). To investigate the H. pylori-induced IL-8 expression on the transcriptional level, we transiently transfected gastric epithelial cells (AGS) with a human IL-8 luciferase reporter construct.The results of this study demonstrate that specifically the C-terminal coiled-coil region of the H. pylori CagL protein, a protein described to be located on the tip of the T4SS-pilus, is responsible for several in vitro observations: 1) H. pylori-induced IL-8 secretion via the transforming growth factor (TGF)-α activated epidermal growth factor-receptor (EGF-R) signaling pathway; 2) H. pylori-induced elongation of the cells, a typical CagA-induced phenotype; and 3) the bridging of the T4SS to its human target cells. This novel bacterial-host recognition sequence allows a new insight into how H. pylori induces the inflammatory response in gastric epithelial cells and facilitates the development of precancerous conditions.

Duodenal ulcer promoting gene 1 (dupA1) is associated with A2147G clarithromycin-resistance mutation but not interleukin-8 secretion from gastric mucosa in Iraqi patients

Helicobacter pylori causes peptic ulceration and gastric adenocarcinoma. The aims were to study the influence of dupA1 positivity upon interleukin-8 (IL-8) secretion from gastric mucosa and determine the prevalence of mutations responsible for clarithromycin and fluoroquinolone resistance. DNA was extracted from 74 biopsies and the virulence factors were studied. Levels of IL-8 in gastric mucosa were measured using ELISA and the mutations responsible for clarithromycin and fluoroquinolone resistance were determined using a GenoType-HelicoDR assay. The prevalence of cagA in strains isolated from gastric ulcer (GU) and duodenal ulcer (DU) was significantly higher than those isolated from non-ulcer disease (NUD) (90% and 57.9% versus 33.3%; p 0.01). The vacA s1m1 genotype was more prevalent in patients with DU (73.7%) and GU (70%) than in those with NUD (13.3%) (p 0.01). The prevalence of dupA1 was higher in DU patients (36.8%) than those with GU (10%) and NUD (8.9%) (p 0.01). Multivariate analysis showed that a cagA+/vacA s1i1m2 virulence gene combination was independently associated with the developing peptic ulcer disease (PUD) with increased odds of developing PUD (p 0.03; OR = 2.1). We found no significant difference in the levels of IL-8 secretion in gastric mucosa infected with H. pylori dupA-negative and H. pylori dupA1-positive strains (dupA-negative: mean ± median: 28 ± 26 versus 30 ± 27.1 for dupA1; p 0.6). While 12 strains were clarithromycin resistant, only three isolates were levofloxacin resistant. A significant association was found between dupA1 genotype and A2147G clarithromycin resistance mutation (p <0.01). Further study is needed to explore the relationship between virulence factors and disease process and treatment failure.

English

Anacardium humile&nbsp;St. Hil.&nbsp;is being used in traditional medicine to treat ulcer. The present work evaluated the mechanisms of action involved in the anti-ulcer properties of the aqueous fraction from leaves of&nbsp;A. humile&nbsp;(AHQ). Gastroprotection of&nbsp;A. humile&nbsp;was evaluated in ethanol and piroxicam models. Mechanisms of action such as mucus production, nitric oxide (NO),&nbsp;sulfhydryl compounds&nbsp;(SH) and the anti-secretory action were evaluated. The acetic acid-induced gastric ulcer model was used to evaluate the&nbsp;A. humilehealing properties. Results obtained in the ethanol model showed that AHQ provided significant gastroprotection at all the tested doses (50, 100, and 200 mg/kg). Thereby, the following protocols were performed using the dose capable of producing the most effective gastroprotection, which was the AHQ 200 mg/kg (P &lt; 0.001). Moreover, AHQ (200 mg/kg) protected the mucosa from piroxicam-induced damage. Mucus, NO, and SH did not participate on this gastroprotection. AHQ interfere in H+&nbsp;secretion in gastric mucosa, thus exerting an anti-secretory activity. Our results suggest that the gastroprotection and cicatrisation process executed by AHQ occurred due to its anti-secretory activity. This study reinforces its traditional medicinal use. Considering that the current therapies are based on the use of anti-secretory agents, the&nbsp;A. humile&nbsp;arises as a promising alternative antiulcer therapy. &nbsp; Key words:&nbsp;Anacardium humile&nbsp;St. Hil., gastric ulcer, gastroprotection.

Gastroprotective and ulcer healing effects of essential oil from Hyptis spicigera Lam. (Lamiaceae)

Hyptis Jacq. (Lamiaceae) is being used in traditional medicine to treat fever, inflammation and gastric disturbances. Hyptis spicigera Lam. is a native plant distributed across the central region of Brazil. The essential oil extracted from this plant is used in folk medicine as antipyretic. The effects of the essential oil obtained from the aerial parts of Hyptis spicigera (OEH) were evaluated for their gastroprotective and healing activities. OEH chemical composition was analyzed by gas chromatography-mass spectrometry (GC-MS). The gastroprotective action of the OEH was evaluated in rodent experimental models (ethanol and NSAID). To elucidate mechanisms of action, the antisecretory action and involvements of NO, SH, mucus and PGE2 were evaluated. The acetic acid-induced gastric ulcer model and Western Blot assay (COX-2 and EGF) were also used to evaluate the OEH healing capacity. GC-MS analysis of OEH indicated three monoterpenes as major compounds: alpha-pinene (50.8%), cineole (20.3%) and beta-pinene (18.3%) and, at the dose of 100 mg/Kg, p.o., OEH provided effective gastroprotection against lesions induced by absolute ethanol (97%) and NSAID (84%) in rats. OEH do not interfere with H+ secretion in gastric mucosa and its gastric protection does not depend on nitric oxide (NO) and sulfhydryl compounds (SH). The gastroprotective action of OEH occurs due to an increase in the gastric mucus production (28%) induced by PGE2 levels. Furthermore, OEH demonstrated a great healing capacity with 87% of reduction in ulcerative lesion area. It accelerated the healing of acetic acid-induced gastric lesions due to an increase in COX-2 (75%) and EGF (115%) expression in gastric mucosa. No sign of toxicity was observed in this study, considering the analyzed parameters. All these results suggest the efficacy and safety of Hyptis spicigera in combating and healing gastric ulcer. Considering the results, it is suggested that the OEH could probably be a good therapeutic agent for the development of new phytotherapeutic medicine for the treatment of gastric ulcer.

Ascorbic acid secretion in the human stomach and the effect of gastrin.

AIM:To investigate the changes of gastric mucosal ascorbic acid secretion in patients with nonulcer dyspepsia and the effect of gastrin on it, and to relate any observed changes to H.pylori infection and mucosal histology.METHODS:Ascorbic acid secretions in patients were examined by collecting continuously gastric juice for one hour after having aspirated and discarded fasting gastric juice. Using the clearance rate (mL/min) of ascorbic acid from blood to gastric juice represented ascorbic acid secretion in the gastric mucosa.Ascorbic acid concentrations in plasma and juice were measured by ferric reduced method.RESULTS:Gastric ascorbic acid secretions in H.pylori-positive patients (1.46mL/min,range 0.27-3.78) did not significantly differ from those in H.pylori-negative patients(1.25mL/min, 0.47-3.14)(P>0.05). There were no significant differences in ascorbic acid secretions between patients with mild (1.56mL/min, 0.50-3.30), moderate (1.34mL/min, 0.27-2.93) and severe (1.36mL/min, 0.47-3.78) inflammation (P >0.05). There were no significant differences in ascorbic acid secretions between patients without activity (1.45mL/min, 0.27-3.14) and with mild (1.32mL/min, 0.61-2.93), moderate (1.49mL/min, 0.50-3.78) and severe (1.43mL/min, 0.51-3.26) activity of chronic gastritis either (P>0.05). Ascorbic acid secretions in patients with severe atrophy (0.56mL/min, 0.27-1.20) were markedly lower than those in patients without atrophy (1.51mL/min, 0.59-3.30) and with mild (1.43mL/min, 0.53-3.78) and moderate (1.31mL/min,0.47-3.16)atrophy(P<0.005). There was a significant negative correlation between ascorbic acid secretion and severity of atrophy (correlation coefficient =-0.43, P<0.005). After administration of pentagastrin, ascorbic acid secretions were markedly elevated (from 1.39mL/min, 0.36-2.96 to 3.53mL/min, 0.84-5.91) (P <0.001).CONCLUSION:Ascorbic acid secretion in gastric mucosa is not affected by H.pylori infection. Gastric ascorbic acid secretion is markedly related to the severity of atrophy, whereas not related to the severity of inflammation and activity. Gastrin may stimulate gastric ascorbic acid secretion. A decreased ascorbic acid secretion may be an important factor in the link between atrophic gastritis and gastric carcinogenesis.

Electroneutral Acid Secretion in Frog Gastric Mucosa: An Electron Microprobe Analysis

To elucidate the mode of H secretion in the intact gastric mucosa, the cellular element concentrations and Rb uptake by individual surface and oxyntic cells of the short-circuited isolated frog gastric mucosa <i>(Rana esculenta, Rana temporaria) </i>were determined using electron microprobe analysis. The H secretion rate was measured by the pH stat method. Under normal conditions both surface and oxyntic cells exhibited typical cellular electrolyte patterns with low Na and high K concentrations. The apical parts of surface cells, in which large mucus-containing vesicles are located, were characterized by relatively high S and Ca concentrations. Histamine-stimulated H secretion in the gastric mucosa of R. <i>esculenta </i>and <i>R. temporaria </i>was about 2.0 and 0.5 µmol/cm²·h, respectively. In the presence of 20 m<i>M</i> Rb in the mucosal bathing solution, a substantial portion of cellular K was exchanged for Rb in oxyntic but not in surface cells. This K-Rb exchange was almost completely abolished by inhibition of H secretion with omeprazole indicating a specific H-Rb(K) exchange across the apical membrane of oxyntic cells. At a low H secretion of about 0.5 µmol/cm²·h about 70% of the H secretion rate could be matched by the omeprazole-inhibitable Rb uptake rate. Accordingly H secretion seems to be accomplished by an electroneutral H-Rb(K) exchange. The negligible Rb uptake into oxyntic cells at a mucosal Rb concentration of 5 m<i>M</i> might be explained by K recirculation across the mucosal membrane via a K conductance and the H-K-ATPase.

SCN − and HSCN transport through lipid bilayer membranes : A model for SCN − inhibition of gastric acid secretion

Diffusion of thiocyanate (SCN −) and thiocyanic acid (HSCN) (p K=−1.8) through lipid bilayer membranes was studied as a function of pH. Membranes were made of egg phosphatidylcholine or phosphatidylcholine plus cholesterol (1:1 mol ratio) dissolved in decane or tetradecane. Tracer fluxes and electrical conductances were used to estimate the permeabilities to HSCN and SCN −. Over the pH range 1.0 to 3.3 only HSCN crosses the membrane at a significant rate. The relation between the total SCN flux ( J A), concentrations and permeabilities is: 1/ J A=1/ P ul([A −]+[HA])+1/ P HA m[HA], where [A −] and [HA] are the concentrations of SCN − and HSCN, P ul is permeability coefficient of the unstirred layer, and P HA m is the membrane permeability to HSCN. By fitting this equation to the data we find that P HA m = 2.6 cm · s −1 and P ul = 9.0 · 10 −4 cm · s −1. Conductance measurements indicate that P A − m is 5 · 10 −9 cm · s −1. Addition of cholesterol to phosphatidylcholine (1:1 mol ratio) reduces P HA m by a factor of 0.4 but has no effect on P A − m. SCN − is potent inhibitor of acid secretion in gastric mucosa, but the mechanism of SCN − action is unknown. Our results suggest that SCN − acts by combining with H + in the mucosal unstirred layer (secretory pits) and diffusing back into the cells as HSCN, thus dissipating the proton gradient across the secretory membrane. A similar mechanism of action is proposed for some other inhibitors of gastric acid secretion, e.g. nitrite (NO 2 −), cyanate (CNO −) and NH 4 +.

Effect of nitrites and nitrates on irrigation and secretion of gastric mucosa in rat.

An aspect of the vasomotor effect of nitrites and nitrates was studied by investigating the influence of these substances on the mucosal blood flow and hence on gastric secretion in the rat. Firstly, point measurements were obtained using an aminopyrine clearance technique after intravenous nitrite and nitrate treatment. Then with an appreciably different technique (14C-aniline clearance on perfused stomach) the kinetics of the phenomenon were followed after, firstly, intravenous administration of the two agents and secondly their intragastric administration. It is interesting to note that nitrites and nitrates are active to differing degrees and present opposing effects: nitrites decrease whereas nitrates globally enhance the factors under consideration (gastric mucosal blood flow, gastric juice volume, acory effect and cuase no modification on intragastric administration. The flow rate-gastric parameter correlations are significant in all cases and show modifications of the aqueous compartments of the body.

ANTI SECRETORY EFFECT OF IMIDAZOLE AND ITS DERIVATIVES IN AN ISOLATED GASTRIC MUCOSA PREPARATION AND AN ANESTHETIZED YOUNG CHICKEN PREPARATION; COMPARISON WITH A HISTAMINE H2-RECEPTOR ANTAGONIST

We invesigated the influences of imidazole on the basal and the secretagogue-stimulated gastric acid secretion in isolated bullfrog gastric mucosa preparations and in anesthetized young chickens. Imidazoles (1 x 10(-4) g/ml) readily depressed the basal acid secretion in gastric mucosa in vitro. The inhibitory effect of imidazole was diminished considerably after washing out of the drug. The maximum acid secretion elicited by tetragastrin or bethanechol was completely antagonized by imidazole (1 x 10(-4) g/ml). The stimulatory action of histamine or dibutyryl cyclic AMP was also remarkably depressed in the presence of imidazole (3 x 10(-4) g/ml). after dibenamine pretreatment (5 x 10(-5) g/ml) for 60 min, the isolated gastric mucosa preparation became refractory to tetragastrin, bethanechol and histamine, but responded to dibutyryl cyclic AMP. Imidazole protected the histamine sensitivity against dibenamine blockade in the concentration of 5 x 10(-4) g/ml. In anesthetized young chickens, imidazole (200 mg/kg, s.c.) depressed tetragastrin- and histamine-stimulated gastric acid secretion. The effects of the imidazole derivatives and several antagonists (metiamide, atropine, diphenhydramine, acetazolamide and 2,4-dinitrophenol) on acid production were compared with that of imidazole. From these results, it is concluded that imidazole has a potent antisecretory effect on the basal and the secretagogue-stimulated acid secretion.

The energetic coupling of acid secretion in gastric mucosa.

The relation between acid secretion and oxidative metabolism has been investigated using nondestructive optical techniques to monitor the redox level of respiratory chain components in the intact, isolated bull-frog gastric mucosa. High rates of acid secretion are found to be associated with cytochrome reduction while inhibition of secretion results in oxidation of the respiratory chain components. Changes in chloride secretion, independent of hydrogen ion secretion, result in opposite cytochrome redox changes indicating that the interaction with oxidative metabolism differs for the two secretory processes. Measurement of intracellular pH changes using indicator dyes shows a correlation between cytochrome reduction and increased pH. The results suggest that there exists a close coupling between the respiratory chain components and hydrogen ion secretion and that this coupling may involve changes in intracellular pH rather than changes in high energy phosphate compounds as previously suggested.

Phospholipid turnover and ultrastructural changes in resting and secreting bullfrog gastric mucosa

1. 1. Ultrastructural changes and 32P 1 incorporation into phospholipids were studied in resting and histamine-stimulated bullfrog gastric mucosae. 2. 2. The relatively smooth apical surface of the resting oxyntic cell becomes engrossed with elaborate microvilli with the onset of acid secretion induced by histamine. These membranous alterations occur presumably at the expense of the abundant smooth endoplasmic reticulum present in the oxyntic cells. Our observations thus confirm the previous findings of other investigators. 3. 3. The ultrastructural changes were accompanied by an increase in the incorporation of 32P 1 into the phospholipid fraction of the histamine-stimulated mucosae, but did not involve a significant net synthesis of lipids. 4. 4. There was a 2–5-fold enhanced incorporation of 32P 1 into phosphatidyl choline and phosphatidyl ethanolamine, and a smaller change in incorporation into phosphatidic acid and phosphatidyl inositol in the mucosae stimulated by histamine. Phosphatidyl serine and sphingomyelin showed relatively little 32P 1 incorporation. 5. 5. Thiocyanate, an inhibitor of acid secretion, abolished the enhanced 32P 1 incorporation into the specific phospholipids. 6. 6. Changes in 32P 1 incorporation into ATP and acid-soluble phosphate ester fraction of the stimulated mucosae were variable. However, even the greatest change observed was not sufficient to account for the large changes observed in specific phospholipids. 7. 7. [2- 14C]Acetate was incorporated to varying degrees into different phospholipids; the greatest incorporation occurred in phosphatidyl choline. However, histamine stimulation did not significantly alter the incorporation of 14C into any of the phospholipids. 8. 8. The increased turnover of the polar groups of phospholipids thus appears to be correlated with alterations and movements of membranous structures concomitant with the histamine-induced acid secretion in gastric mucosa.

Behavior of the nitrate ion in the dog.

ArticleBehavior of the Nitrate Ion in the DogInez Greene, and E. P. HiattInez GreeneFrom the Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, North Carolina, and E. P. HiattFrom the Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, North CarolinaPublished Online:28 Feb 1954https://doi.org/10.1152/ajplegacy.1954.176.3.463MoreSectionsPDF (949 KB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByNitrite as undesirable substances in animal feed ‐ Scientific Opinion of the Panel on Contaminants in the Food ChainEFSA Journal, Vol. 7, No. 4Nitric oxide, inducible nitric oxide synthase and inflammation in veterinary medicine9 March 2007 | Animal Health Research Reviews, Vol. 3, No. 2Nitric oxide metabolites in naturally occurring canine babesiosisVeterinary Parasitology, Vol. 104, No. 1Plasma Nitrate Accumulation during the Development of Pacing-Induced Dilated Cardiac Myopathy in Conscious Dogs Is Due to Renal ImpairmentNitric Oxide, Vol. 5, No. 1Renal handling of circulating nitrates in anesthetized dogsMurrell Godfrey, and Dewan S. A. Majid1 July 1998 | American Journal of Physiology-Renal Physiology, Vol. 275, No. 1Water Quality I: The Effect of Water Nitrate and pH on Broiler Growth PerformanceJournal of Applied Poultry Research, Vol. 5, No. 4Human exposure, pharmacology and metabolism of nitrate and nitriteBiotransformation of nitric oxide.Environmental Health Perspectives, Vol. 73Nitrate formation in rats exposed to nitrogen dioxideToxicology and Applied Pharmacology, Vol. 67, No. 2Urinary catecholamine metabolites (vanylmandelic and homovanillic acds) in the rat after subchronic treatment with sodium nitrate or nitriteExperientia, Vol. 38, No. 4Nitrates and Nitrites: Ingestion, Pharmacodynamics, and ToxicologyNitrate, nitrite and N-nitroso compounds: biochemistry, metabolism, toxicity and carcinogenicityFate of Ingested 15 N-Labelled Nitrate and Nitrite in the RatJournal of Food Science, Vol. 46, No. 3Endogenous Carcinogenesis: Nitrate, Nitrite and N-Nitroso CompoundsDistribution and metabolism of ingested NO3- and NO2- in germfree and conventional-flora ratsApplied and Environmental Microbiology, Vol. 38, No. 5Distribution of nitrogen-13 from labeled nitrate and nitrite in germfree and conventional-flora ratsApplied and Environmental Microbiology, Vol. 38, No. 5Effect of nitrites and nitrates on irrigation and secretion of gastric mucosa in ratNaunyn-Schmiedeberg's Archives of Pharmacology, Vol. 309, No. 1Response : Nitrate and Nitrite: Origin in HumansScience, Vol. 205, No. 4413Erratum: Obstetrical Medication StudyScience, Vol. 205, No. 4413Erratum: Dynamics of Skeletal Pattern Formation in Developing Chick LimbScience, Vol. 205, No. 4413Nitrite and Nitrate Are Formed by Endogenous Synthesis in the Human IntestineScience, Vol. 200, No. 4349Nitroglycerin Revisited: Chemistry, Biochemistry, Interactions22 September 2008 | Drug Metabolism Reviews, Vol. 4, No. 1Recent Views on the Mechanisms of Nitrate Ester Metabolism22 September 2008 | Drug Metabolism Reviews, Vol. 2, No. 1Nitrates as an Environmental, Animal, and Human Hazard25 September 2008 | Clinical Toxicology, Vol. 7, No. 2Metabolism of Ethylene Glycol Dinitrate and its Influence on the Blood Pressure of the RatOccupational and Environmental Medicine, Vol. 24, No. 4Physiologische Chemie der Lebensvorgänge und OrganePhysiology of the kidneyNitrate Accumulation In Crops And Nitrate Poisoning In AnimalsNitrate Content of Beets, Collarets, Turnip GreensJournal of the American Dietetic Association, Vol. 43, No. 1Die Nierenhämodynamik als natriumbewahrendes PrinzipZeitschrift für Die Gesamte Experimentelle Medizin, Vol. 136, No. 1PLASMA NITRATE AND NITRITE CONCENTRATION IN CHRONIC AND ACUTE NITRATE POISONING IN SHEEPAustralian Veterinary Journal, Vol. 38, No. 2Effect of potassium nitrate solutions on blood pressure of ratsThe American Journal of Cardiology, Vol. 8, No. 5The Effects of Dietary Nitrate on Rabbits and RatsThe Journal of Nutrition, Vol. 69, No. 1Die Bedeutung des Nitratgehaltes von Gem�se in der Ern�hrung des S�uglingsZeitschrift f�r Kinderheilkunde, Vol. 81, No. 4CHLORIDE CONTENT AND METABOLISM OF CEREBRAL TISSUES IN FLUIDS LOW IN CHLORIDESJournal of Neurochemistry, Vol. 1, No. 1 More from this issue > Volume 176Issue 3February 1954Pages 463-467 Copyright & PermissionsCopyright © 1954 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1954.176.3.463PubMed13138739History Received 21 August 1953 Published online 28 February 1954 Published in print 28 February 1954 Metrics