Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Congenital chloride diarrhoea is an autosomal recessive disease characterized by life-long watery diarrhoea of prenatal onset with high faecal Cl- concentration. Seventy-nine patients have so far been reported. The basic defect involves the active Cl-/HCO3- exchange mechanism of the distal ileum and colon. The defect causes impaired absorption of Cl-, acidity of intestinal contents because of impaired excretion of HCO3-, and, secondarily, impaired Na+ absorption. Intra-uterine diarrhoea leads to hydramnios and often to premature birth. Unless adequately treated, most patients will die of hypo-electrolytaemic dehydration within the 1st few months of life. Some infants will survive in such a state, with severe alkalosis, hypochloraemia, hypokalaemia, and retarded growth and development. Their plasma renin and aldosterone concentrations will become grossly elevated, and pathological changes will develop in the kidneys. The diagnosis is established when faecal Cl- concentration exceeds 90 mmol/l after water and electrolyte deficits have been corrected. Congenital chloride diarrhoea should be treated with full oral replacement of the faecal losses of Cl-, Na+, K+, and water. This therapy will abolish all the secondary disorders, provide for normal growth and development, and prevent renal disease. Though this therapy does not abolish the diarrhoea, most children will become toilet trained at a normal age, their social adjustment will be unimpaired, and they will live a perfectly normal life.
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PMID:Congenital chloride diarrhoea. 352 96

The ionic compensatory response to CO2 breathing for 3 days was studied on intact and cystectomized turtles at 10 and 20 degrees C. Arterial blood gases, pH, ionized calcium, and the plasma concentrations of Na+, K+, Cl-, total Ca2+, and total Mg2+ were measured periodically. At 20 degrees C, ureteral urine was also collected from bladderless turtles and was analyzed for pH, ions, NH3+, total CO2, osmolality, and titratable acid. When CO2 was breathed there was a compensatory change in the strong-ion difference as manifest by an increase in plasma [HCO3-] that was approximately 10 meq/l both in the 10 and 20 degrees C turtles. The only significant associated strong-ion changes observed consistent with the ionic compensatory response were increases in total and ionized Ca2+ and total Mg2+. These results were unaffected at either temperature by surgical removal of the urinary bladder. Urine collected from cystectomized turtles showed no compensatory increase in acid excretion during hypercapnia; in fact, changes occurred in the opposite direction. Urinary excretion of HCO3- and urine pH increased significantly, whereas titratable acidity decreased significantly. No significant change occurred in ammonia excretion over the three days of hypercapnia. These data argue against compensatory roles for the kidneys and urinary bladder in this species and point to internal ionic exchanges involving bone and shell.
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PMID:Ionic compensation with no renal response to chronic hypercapnia in chrysemys picta bellii. 378 4

Sham feeding (SF) was used to evaluate the effect of physiological vagal stimulation on gastric acid (H+) and bicarbonate (HCO3-) secretion in humans, as well as on parietal and nonparietal volume secretion. A recently validated method, derived from a two-component model of gastric secretion, was employed. SF increased both H+ secretion from parietal cells (P less than 0.001) and HCO3- secretion from nonparietal cells (P less than 0.01), although the H+ response was greater and more prolonged. Atropine significantly inhibited not only H+ secretion but also HCO3- and nonparietal volume secretion. Peak H+ secretion during SF averaged approximately 27 mmol/h, whereas peak HCO3- secretion averaged approximately 6 mmol/h. When H+ secretion was already maximally stimulated by an intravenous pentagastrin infusion, SF actually reduced gastric juice acidity and osmolality due to neutralization of H+ by HCO3- and to dilution of H+ by nonparietal secretions. These studies therefore indicate that vagal stimulation induced by SF increases both H+ and HCO3- secretion in humans and that this process is cholinergically dependent.
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PMID:Gastric H+ and HCO3- secretion in response to sham feeding in humans. 397 Jan 99

Acid secretion by the stomach is enhanced by H2 histamine stimulation and is depressed by its inhibition. The present investigation was undertaken to assess the possible effect of H2 histamine activity on acid excretion by the kidney, the other major acid secreting organ. The study was stimulated by an earlier observation indicating a fall in urinary acid excretion in human associated with short-term administration of an H2 histamine antagonist (cimetidine). Female Sprague-Dawley rats were randomly assigned to the cimetidine-treated, histolog-treated and placebo-treated (control) groups. Urinary titratable acidity, NH4+, HCO3- and net acid excretion rates were determined following administration of either cimetidine, histolog or placebo. Excepting the above pharmacologic manipulations all other experimental conditions were similar. Urinary titratable and net acid excretion rates were significantly reduced with cimetidine and increased with histalog as compared with the control group. The observed urinary changes are not due to the effects of these agents on gastric acid secretion since if that was the case the opposite results would have been expected. The data suggest that urinary acidification is somehow influenced by acute changes of H2 histamine activity in rats. The precise mechanism, site of action in the kidney and pathophysiologic significance of this phenomenon remains to be elucidated.
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PMID:Effect of H2 histamine receptor blockade and stimulation on urinary acidification. 408 82

Preliminary experiments established that a 0.5-ml inoculum that is introduced directly into the stomach of mice was cleared rapidly into the small intestine. Bicarbonate buffer, but not skim milk, protected such an inoculum from stomach acid until at least 90% of it had entered the small intestine. Passage and survival of various Escherichia coli strains through the mouse gut were tested by introducing a buffered bacterial inoculum directly into the stomach, together with the following two intestinal tracers: Cr(51)Cl(3) and spores of a thermophilic Bacillus sp. Quantitative recovery of excreted bacteria was accomplished by collecting the feces overnight in a refrigerated cage pan. The data show that wild-type E. coli strains and E. coli K-12 are excreted rapidly (98 to 100% within 18 h) in the feces without overall multiplication or death. E. coli varkappa1776 and DP50supF, i.e., strains certified for recombinant DNA experiments underwent rapid death in vivo, such that their excretion in the feces was reduced to approximately 1.1 and 4.7% of the inoculum, respectively. The acidity of the stomach had little bactericidal effect on the E. coli K-12 strain tested, but significantly reduced the survival of more acidsensitive bacteria (Vibrio cholerae) under these conditions. Long-term implantation of E. coli strains into continuous-flow cultures of mouse cecal flora or into conventional mice was difficult to accomplish. In contrast, when the E. coli strain was first inoculated into sterile continuous-flow cultures or into germfree mice, which were subsequently associated with conventional mouse cecal flora, the E. coli strains persisted in a large proportion of the animals at levels resembling E. coli populations in conventional mice. Metabolic adaptation contributed only partially to the success of an E. coli inoculum that was introduced first. A mathematical model is described which explains this phenomenon on the basis of competition for adhesion sites in which an advantage accrues to the bacterium which occupies those sites first. The mathematical model predicts that two or more bacterial strains that compete in the gut for the same limiting nutrient can coexist, if the metabolically less efficient strains have specific adhesion sites available. The specific rate constant of E. coli growth in monoassociated gnotobiotic mice was 2.0 h(-1), whereas the excretion rate in conventional animals was -0.23 h(-1). Consequently, limitation of growth must be regarded as the primary mechanism controlling bacterial populations in the large intestine. The beginnings of a general hypothesis of the ecology of the large intestine are proposed, in which the effects of the competitive metabolic interactions described earlier are modified by the effects of bacterial association with the intestinal wall.
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PMID:Survival and implantation of Escherichia coli in the intestinal tract. 633 89

It is known that Pi normally provides the major source of non-NH3 urinary buffer and that Pi-buffered renal H+ excretion (titratable acidity, TA) accounts for a large fraction of daily renal net acid excretion (NAE). Whether the presence of luminal non-NH3 buffers is a prerequisite to normal renal regulation of systemic acid-base equilibrium under any conditions has not been investigated. Accordingly, I investigated whether chronic renal regulation of plasma (p) [HCO3] might be impaired under conditions of normophosphatemic hypophosphaturia (NHP) produced by short-term dietary Pi restriction. During a steady-state of HCl-induced acidosis in NaCl-replete NHP dogs (group 1A, N = 6), [HCO3-]p averaged 14.1 +/- 0.6 mEq/liter and arterial (a) [H+] averaged 54 +/- 2 nEq/liter. Substitution K+ 2.5 mEq/kg as neutral Pi for equivalent dietary KCl for 7 to 8 days resulted in significant amelioration of acidosis (delta [HCO3-]p + 2.2 +/- 0.5 mEq/liter, P less than 0.01; delta [H+]a -6 +/- 2 nEq/liter, P less than 0.01) in association with a cumulative increment (sigma delta) in TA excretion (+ 103 mEq, P less than 0.001) and NAE (+ 22 mEq). To investigate whether Pi-induced amelioration of acidosis was related to enhanced urinary buffer capacity, an additional group (group 1B, N = 5) with NHP and chronic HCl acidosis was administered the non-Pi buffer, neutral creatinine (5.0 mmoles/kg daily). As with Pi, acidosis was ameliorated by creatinine administration and sigma delta NAE increased.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypophosphaturia impairs the renal defense against metabolic acidosis. 651 76

A pH gradient is maintained at the surface of rat duodenum exposed to luminal acid. The alkalinity and thickness of this gradient are dependent on the rate of surface epithelial HCO3- secretion (transport into the lumen). Acidification of the luminal solution stimulates HCO3- secretion and enhances the alkalinity at the mucosal surface by a mechanism dependent on endogenous prostaglandin synthesis. This stimulated HCO3- secretion is quantitatively sufficient to maintain neutrality at the epithelial surface of the mucosa even in the presence of as high luminal acidity as pH 2.0, which is the maximal 'physiologic' acidity within human duodenal bulb. Exogenous prostaglandin E2 increases HCO3- secretion as well as the dimensions of the pH gradient, which may, in part, account for its cytoprotective actions in gastroduodenal mucosa. The findings suggest that epithelial HCO3- secretion in the duodenal mucosa has a protective function by forming an unstirred alkaline layer at the mucosal surface which impedes the diffusion of luminal acid into the mucosa.
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PMID:HCO3- secretion and surface pH gradient in rat duodenum exposed to luminal acid. 658 36

The microvasculature of the rat forestomach was compared with that of the glandular stomach using scanning electron microscopy of vascular corrosion casts and conventional transmission electron microscopy. The forestomach stratified mucosa is relatively poorly vascularized, having a simple 2 dimensional array of continuous capillaries located subepithelially. This contrasts with the extensive mucosal microvascular network of the glandular stomach, where fenestrated capillaries are closer to adjacent cells. pH measurements were taken at the mid-forestomach luminal surface and midfundic luminal surface of the glandular stomach. The H+ concentration was 200 x lower at the forestomach luminal surface. There was always food within the stomach. The pH of the food bolus, which extended throughout the stomach, reflected the pH of the adjacent mucosa. Because of their microvascular differences, the portal transport of HCO3- purported to protect the glandular mucosa from luminal acidity cannot operate at the forestomach mucosa. We speculate that the low forestomach acidity results from the buffering action of the food bolus and that the anatomically distinct dividing ridge restricts direct access of fundic secretions to the forestomach mucosa.
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PMID:The microvasculature and gastric luminal pH of the forestomach of the rat: a comparison with the glandular stomach. 667 41

Since calcium solubility is a prerequisite to calcium absorption, and since solubility of calcium is highly pH-dependent, it has been generally assumed that gastric acid secretion and gastric acidity play an important role in the intestinal absorption of calcium from ingested food or calcium salts such as CaCO3. To evaluate this hypothesis, we developed a method wherein net gastrointestinal absorption of calcium can be measured after ingestion of a single meal. A large dose of cimetidine, which markedly reduced gastric acid secretion, had no effect on calcium absorption in normal subjects, and an achlorhydric patient with pernicious anemia absorbed calcium normally. This was true regardless of the major source of dietary calcium (i.e., milk, insoluble calcium carbonate, or soluble calcium citrate). Moreover, calcium absorption after CaCO3 ingestion was the same when intragastric contents were maintained at pH 7.4 (by in vivo titration) as when intragastric pH was 3.0. On the basis of these results, we conclude that gastric acid secretion and gastric acidity do not normally play a role in the absorption of dietary calcium. Other possible mechanisms by which the gastrointestinal tract might solubilize ingested calcium complexes and salts are discussed.
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PMID:An evaluation of the importance of gastric acid secretion in the absorption of dietary calcium. 670 97

The effect of a period of induced back diffusion of H+ on the isolated amphibian gastric mucosa was studied under various conditions. Under standard conditions (HCO3--buffered nutrient solution; 95% O2-5% CO2), passage of an electrical current of 500 microA/cm2 for 15 min from a secretory fluid of pH 2.10 across the mucosal resulted in a decrease of the transmucosal potential difference (PD) of 10.9 +/- 1.9 mV, a decrease of resistance (R) of 48 +/- 26 ogema cm2 and a decrease of short circuit current (Isc) of 18 +/- 7 microA/cm2. Flux of the neutral molecule, erythritol from secretory (S) to nutrient (N) fluid increased by 66% and the active transport of Cl- N lead to S decreased from 2.9 to 1.9 microeq/cm2/hr. With removal of HCO3- from the nutrient fluid and with inhibition of carbonic anhydrase activity the period of back diffusion induced significantly greater change in the electrical measurements than occurred when under standard conditions. This increased effect of back diffusion of H+ was not changed by change of the nutrient fluid pH from 7.20 to either 6.6 or 8.2. Increase of the HCO3- concentration of the nutrient fluid to 35 mM or decrease of the CO2 content of the aerating gas to 1% were associated with significantly less change of the electrical measurements than occurred with standard conditions. These studies support the proposal that the the neutralizing reaction HCO3- + H+ leads to CO2 + H2O plays a central role in the gastric mucosal handling of backing diffusing H+ and suggests that the capacity and poise of the HCO3-/CO2 buffer system is an important determinant of the ability of the mucosa to tolerate luminal acidity.
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PMID:Role of acid-base status in the response of the isolated amphibian gastric mucosa to back diffusion of H+. 677 1


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