Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0003129 (Anoxia)
 551 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

1. The transport of HCO3- (Jsm) from a HCO3(-)-buffered serosal to an unbuffered mucosal saline solution has been studied in rat caecum in vitro. 2. Carbachol, bethanechol and acetylcholine (ACh) caused a concentration-dependent fall in Jsm with similar maximum effects. 1,1-Dimethyl-4-phenyl-piperazinium iodide (DMPP) also inhibited Jsm but the effect was less than with the other drugs. Maximum cholinoceptor inhibition was less than that obtained with anoxia. 3. Responses were blocked by atropine (10(-5) M) but hexamethonium (2 x 10(-4) M) significantly altered the response only to DMPP. 4. Physostigmine (10(-5) M) shifted the ACh response curve to the left but physostigmine itself caused inhibition of Jsm which was blocked by atropine. 5. Substitution of mucosal Cl- by NO3- reduced Jsm to a similar extent to maximum cholinoceptor effect and abolished responses to bethanecol. Anoxia further reduced Jsm in the presence of NO3-. 6. Mucosal SITS and DIDS (1 mM) reduced Jsm but this was less than the maximum inhibition seen with drugs acting on cholinoceptors or mucosal Cl- removal. Serosal DIDS caused a similar inhibition. 7. We conclude that cholinoceptor agonists inhibit but do not abolish luminal bicarbonate transport by an action on muscarinic receptors.
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PMID:The effect of drugs acting on cholinoceptors and mucosal chloride on luminal bicarbonate transport by rat caecum under in vitro conditions. 188 14

Under in vitro conditions the rat cecum transported HCO3- from the serosal to an unbuffered solution in contact with the mucosal side [Js----m = 7.12 +/- 0.18 mumol.cm-2.h-1 (n = 149)]. With reversed tissues, a significantly lower flux was obtained [Jm----s = 2.47 +/- 0.11 mumol.cm-2.h-1 (n = 42)]. Both fluxes were stable for several hours. Increasing the H+ gradient across the tissue for 60 min did not change either flux. Anoxia for 45 min reversibly reduced Js----m by 65 +/- 3% (n = 20) but had no effect on Jm----s. Both fluxes were linearly related to HCO3- concentration on the buffered side, but the slope for Js----m was 3.5 times that for Jm----s. When tissues were initially set up in HEPES buffer rather than HCO3-, Js----m was 0.12 +/- 0.05 mumol.cm-2.h-1 (n = 6), which is not significantly different from zero. Replacement of Na+ by choline reduced Js----m by 40 +/- 3% (n = 11) and ouabain (1 mM) by 24 +/- 3% (n = 5). Replacement of Cl- with isethionate or K+ with Na+ for 60 min did not alter Js----m. Serosal application of DIDS (0.5 mM) reduced Js----m by 24 +/- 6% (n = 6), but SITS (0.5 mM), furosemide (1 mM), acetazolamide (0.1 mM), amiloride (1 mM), and a proton pump inhibitor (Sch 28080, 50 microM) had no effect. Mucosal application of DIDS, furosemide, and amiloride had no effect on Js----m. Serosal tetrodotoxin (1 microM) and indomethacin (28 microM) were also without effect.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Characteristics of luminal bicarbonate secretion by rat cecum in vitro. 190 Jun 75

Net Cl- absorption by Amphiuma small intestine is electrogenic but associated with the secretion of HCO3-. To define the mechanisms of Cl- entry into the enterocytes the initial rate of uptake of 36Cl into isolated segments of small intestine was measured. Luminal extracellular space was measured using [3H]inulin. Cl- influx was saturable with a Km of 5.3 mM. When the mucosal medium Cl- concentration was 20 mM influx was linear for 5 min. Cl- influx in 5 min (JiCl) was not reduced by 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid added to the serosal medium, although the Cl- current was abolished. Hence the luminal membrane was the barrier to Cl- uptake. Monovalent anions blocked Cl- influx in the order I- = SCN- = NO3- greater than Br- greater than F-. Anoxia and dinitrophenol reduced JiCl 33 and 71%, respectively. Substitution of medium Na+ with choline or N-methyl glucamine reduced JiCl 60-70%. Removal of medium K+ reduced influx 51%. After medium Na+ and K+ were both replaced influx was stimulated upon reexposure to (Na+ + K+); Na+ alone did not stimulate. JiCl was reduced 34% by furosemide. Neither amiloride nor SITS in the mucosal medium altered influx. JiCl was reduced by replacement of the HCO3- -CO2 buffer with either phosphate or N-2-hydroxyethyl-piperazine-N'-2-ethanesulfonic acid and by exposure to acetazolamide. Theophylline reduced influx 60%, whereas the Ca ionophore A23187 reduced net Cl- absorption and lowered JiCl by 17%. Norepinephrine (10(-5) M) in the serosal bathing medium stimulated Cl- influx 51%. These results indicate that Cl- influx into the intestinal mucosa occurs by a Na+- and, possibly, K+-dependent pathway. Cl- entry is under adrenergic influence.
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PMID:Characteristics of chloride ion influx in Amphiuma small intestine. 253 36

The relations among alkaline secretion, short-circuit current (Isc), and fluxes of Na+ and Cl- are examined. The Isc (1.15 +/- 0.03 microeq.cm-2.h-1) was significantly greater than the rate of alkaline secretion (1.02 +/- 0.02 microeq.cm-2.h-1). Regression analysis (n = 300) showed a highly significant correlation between alkaline secretion and Isc and indicated a residual Isc of 0.26 microeq.cm-2.h-1. In the absence of HCO3-, there was a residual Isc of 0.25 +/- 0.04 microeq.cm-2.h-1. This residual Isc is accounted for by an observed net Na+ absorption of 0.28 +/- 0.04 microeq.cm-2.h-1. Fluxes of Na+ fail to fit the flux-ratio equation and were not significantly affected by 2 X 10(-6) M ouabain, 5 X 10(-5) M amiloride, or anoxia but were significantly reduced by 2,4,6-triaminopyrimidine. The net Cl- flux was not significantly different from zero. Cl- fluxes conform to the flux-ratio equation and were reduced by anoxia or 2,4,6-triaminopyrimidine but were not affected by 4-acetamido-4'-isothiocynostilbene-2,2'-disulfonic acid (SITS). Anoxia or ouabain significantly inhibited alkaline secretion and Isc without affecting net fluxes of Na+ or Cl-, whereas amiloride or SITS had no effect on any of these parameters. There is no NaCl-coupled transport nor anion exchange, but solute-coupled Na+ absorption is demonstrated. We conclude that alkaline secretion by the duodenum involves a transcellular, energy-requiring, Na+-dependent, ouabain-sensitive, electrogenic mechanism that accounts for at least 80% of the Isc. Net Na+ absorption accounts for the residual Isc. Movements of Cl- are passive, do not contribute to Isc, and are not involved in the mechanism of alkaline secretion. Two hypothetical models of transcellular alkaline secretion are proposed.
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PMID:Alkaline secretion by amphibian duodenum. II. Short-circuit current and Na+ and Cl- fluxes. 697 2