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PubMed2002

Intestinal absorption enhancement of the ester prodrug tenofovir disoproxil fumarate through modulation of the biochemical barrier by defined ester mixtures.

The effect of discrete esters and ester mixtures on the intestinal stability and absorption of tenofovir disoproxil fumarate (tenofovir DF, an esterase-sensitive prodrug of the antiviral tenofovir) was compared with the effect of strawberry extract, which has been shown to enhance the absorption of the prodrug across Caco-2 monolayers and in rat ileum. In addition, the mechanism of absorption enhancement was investigated. In rat intestinal homogenates, complete inhibition of the conversion of tenofovir DF (as obtained by strawberry extract) could only be obtained at relatively high concentrations of the discrete esters or by using mixtures of esters (e.g., propyl p-hydroxybenzoate 0.02%, octyl acetate 0.02%, ethyl caprylate 0.01%). Coincubation of tenofovir DF with this mixture also resulted in an enhancement of its absorption in the in vitro Caco-2 system as well as in rat ileum. As tenofovir DF is a substrate for P-glycoprotein (P-gp)-related efflux carriers in the Caco-2 model, the modulatory effect of the ester mixtures was studied on the functionality of P-gp using cyclosporin A (CsA) as a model substrate. Strawberry extract as well as the mixture of three esters interfered with the absorptive transport of CsA across Caco-2 monolayers, illustrating that both mixtures interfere with both esterase-activity and P-gp functionality. This concerted barrier was not observed in rat ileum, suggesting differential functional activities of the biochemical barrier toward tenofovir DF in different absorption systems. Overall, our results illustrate that modulation of the biochemical barrier (metabolism and efflux) of tenofovir DF by ester mixtures can be used to increase the intestinal absorption of tenofovir DF in an in vitro and an in situ absorption model; the mechanism of action appears to be a complex interplay of different systems; the differential expression of carriers and enzymes in different systems illustrates the difficulty of extrapolating observations between different systems/species.

Adenine↗
PubMed2006

A noninflammatory interleukin-1beta fragment stimulates fetal lung fluid absorption in guinea pigs.

We have previously demonstrated that full-length interleukin (IL)-1beta can induce and stimulate lung fluid absorption in near-term guinea pig fetuses via stimulation of fetal cortisol synthesis and release. To develop a potentially clinically useful drug, we tested the hypothesis that maternal administration of a noninflammatory IL-1beta-fragment (IL-1beta(Fr)) induced cortisol synthesis and stimulated lung fluid absorption in preterm fetuses. IL-1beta(Fr) was administered s.c. daily to timed-pregnant guinea pigs for 3 days with and without simultaneous cortisol synthesis inhibition by metyrapone. Fetuses were obtained by abdominal hysterotomy at 61 and 68 days gestation and instilled with isosmolar 5% albumin into the lungs, and lung fluid absorption was measured over 1 h by mass balance. Lung fluid absorption was induced at 61 days and stimulated at 68 days gestation by IL-1beta(Fr), which both were attenuated by cortisol synthesis inhibition. Moreover, induction of labor by oxytocin stimulated lung fluid absorption at 61 days but had no stimulatory effect at 68 days gestation when given with the IL-1beta(Fr). Plasma adrenocorticotropin and cortisol concentrations were increased by IL-1beta(Fr) at 61 days gestation and remained high but unstimulated by IL-1beta(Fr) at 68 days gestation, and metyrapone always reduced cortisol concentrations. Prenatal lung fluid absorption, when present as well as IL-1beta(Fr)-induced, was always propranolol- and amiloride-sensitive, suggesting that beta-adrenoceptor stimulation and the epithelial Na(+) channel (ENaC) were critical for the induced/stimulated lung fluid absorption. ENaC expression was increased by IL-1beta(Fr) and attenuated by cortisol synthesis inhibition. Thus, our results suggest a potential clinical use of IL-1beta(Fr) therapeutically to induce lung fluid absorption in fetuses at risk of preterm delivery.

Absorption↗
PubMed1997

Nonlinear intestinal absorption kinetics of cefuroxime axetil in rats.

Cefuroxime is commercially available for parenteral administration as a sodium salt and for oral administration as cefuroxime axetil, the 1-(acetoxy)ethyl ester of the drug. Cefuroxime axetil is a prodrug of cefuroxime and has little, if any, antibacterial activity until hydrolyzed in vivo to cefuroxime. In this study, the absorption of cefuroxime axetil in the small intestines of anesthetized rats was investigated in situ, by perfusion at four concentrations (11.8, 5, 118 and 200 microM). Oral absorption of cefuroxime axetil can apparently be described as a specialized transport mechanism which obeys Michaelis-Menten kinetics. Parameters characterizing absorption of prodrug in free solution were obtained: maximum rate of absorption (Vmax) = 289.08 +/- 46.26 microM h-1, and Km = 162.77 +/- 31.17 microM. Cefuroxime axetil transport was significantly reduced in the presence of the enzymatic inhibitor sodium azide. On the other hand, the prodrug was metabolized in the gut wall through contact with membrane-bound enzymes in the brush border membrane before absorption occurred. This process reduces the prodrug fraction directly available for absorption. From a bioavailability point of view, therefore, the effects mentioned above can explain the variable and poor bioavailability following oral administration of cefuroxime axetil. Thus, future strategies in oral cefuroxime axetil absorption should focus on increasing the stability of the prodrug in the intestine by modifying the prodrug structure and/or targeting the compound to the absorption site.

Animals↗
PubMed1976

Impairment of jejunal absorption rate of carnosine by glycylglycine in man in vivo.

Using a double-lumen tube jejunal perfusion system in vivo, the mutual effects of carnosine (beta-alanyl-L-histidine) and glycylglycine on their respective absorption rates have been studied in six Zambian African adults. Data on the effect of the constituent amino-acids of carnosine on glycylglycine absorption rate have similarly been obtained. The solutions infused in each subject contained (A) carnosine (50 mmol l.-1), (B) carnosine (50 mmol l.-1) and glycylglycine (50 mmol l.-1), (C) glycylglycine (50 mmol l.-1), and (D) glycylglycine (50 mmol l.-1), L-histidine (50 mmol l.-1) and beta-alanine (50 mmol l.-1). Glycylglycine produced a significant impairment in the mean rate of histidine absorption from carnosine (P less than 0-01). However, carnosine did not have a significant effect on the mean rate of glycine absorption from glycylglycine. Mean rate of histidine absorption from solution D was significantly higher than that from solution A (P less than 0-01). Mean rate of glycine absorption from glycylglycine was not significantly different during infusion of solutions B, C, and D. The results are consistent with the concept that carnosine on glycylglycine is probably because the affinity of mechanism; the lack of influence of carnosine on glycylglycine is probably because the affinity of carnosine for the dipeptide uptake mechanism is relatively low. A gross difference has been shown between mean absorption rate of histidine from free L-histidine (solution D) (25-8 mmol h-1) and when it is given in the form of carnosine in the presence of another dipeptide (solution B) (8-7 mmol h-1); that emphasizes the complexity of amino acid and peptide interaction during absorption, which must be important in nutrition.

Adolescent↗
PubMed1976

Intestinal perfusion studies in tropical sprue. 1. Amino acid and dipeptide absorption.

Intestinal absorption of glycine 20 mmol/1, glycyl-glycine 10 mmol/1 plus L-leucine 10 mmol/1, and glycyl-L-leucine 10 mmol/1 has been studied by intestinal perfusion in 11 patients with tropical sprue and 10 control subjects. The patients with sprue had a significant reduction in the rate of absorption of glycine from a 20 mmol/1 solution, but there were no significant differences in the absorption of the other substances. The failure to demonstrate any difference in the absorption of these substances is probably related to their low concentration relative to the maximum absorptive capacity of the intestine. In both groups of subjects the kinetic advantage of glycyl-glycine absorption as compared with glycine absorption was maintained. When the dipeptides were perfused, free amino acids appeared in the perfusate presumably by "back diffusion" from the mucosal cells. In the case of glycyl-L-leucine considerably more glycine and leucine were found in the perfusate in patients with sprue than in the control subjects. There was no correlation between peptide absorption and the concentration of total glycly-glycine hydrolase and glycyl-L-leucine hydrolase, measured as combined brush border and cytosol enzymes. The concentrations of these enzymes were similar in both groups of subjects.

Amino Acids↗
PubMed1990

Acetate absorption in the normal and secreting rat jejunum.

Acetate absorption was studied in rat jejunum using steady state perfusion in vivo. Absorption conformed to apparent saturation kinetics and was similar in magnitude to glucose absorption. When compared with normal saline, acetate perfusion was associated with luminal alkalinisation. There was no difference in total CO2 secretion when similar rates of acetate and glucose absorption were compared, suggesting that total CO2 secretion was the result of mucosal metabolism. Absorption of acetate and propionate were mutually inhibitory. Acetate absorption was also inhibited by Tris-Hepes pH 7.0. When the gut was pretreated with cholera toxin to induce a secretory state, acetate absorption was reduced by 41.9%. This effect could be reproduced if similar water secretion was osmotically induced by the addition of mannitol. These data suggest that acetate is absorbed, at least, partially by non-ionic diffusion in the rat jejunum and that its absorption is reduced in the secreting intestine by solvent drag.

Acetates↗
PubMed2000

Intestinal failure defined by measurements of intestinal energy and wet weight absorption.

BACKGROUND AND AIMS: Intestinal failure defined by the minimal energy and wet weight absorption required to avoid home parenteral nutrition (HPN) is not well described. Thus the aim of this study was to identify the minimal level of gut function necessary to avoid parenteral support using objective measurements of intestinal function. METHODS: Energy (bomb calorimetry) and wet weight absorption were measured during 48 hour balance studies in 45 HPN patients with intestinal failure and in 44 non-HPN borderline patients with a short bowel or malabsorption exceeding 2 MJ/day. RESULTS: In the non-HPN patients, the lower 5% confidence interval of the absorption of energy was 84% of the basal metabolic rate (BMR, the Harris-Benedict equations), equivalent to 4.9 MJ/day. Wet weight absorption was 1.4 kg/day. The HPN patients absorbed less of either or both. The non-HPN patients absorbed 24-86% (range) of the energy and 23-95% of the wet weight. Absorption in the HPN patients ranged from below 0% (net secretion) in patients with very short bowels to 100% absorption of an insufficient oral intake in patients with pseudo-obstruction. Non-HPN patients who absorbed less than half of their intake avoided HPN by hyperphagia (200-400% of BMR equivalent to 10-24 MJ/day, and 3-7 kg/day of wet weight). CONCLUSION: Intestinal failure was accurately measured as absorption below 1.4 kg/day of wet weight and 84% of the calculated BMR (depending on weight, sex and age), which is equal to 4.9 MJ/day. Intestinal absorption, expressed as a percentage of intake, did not discriminate between patients with and without intestinal failure, except for patients who absorbed less than 25% of their intake.

Adult↗
PubMed1984

Intestinal absorption of free oleic acid in the unanesthetized rat: evidence for a saturable component?

The intestinal absorption of free oleic acid at low intraluminal concentrations and the influence of luminal factors on its absorption were studied in the unanesthetized rat. The relationship between oleic acid concentration (30-2500 microM) and its rate of absorptions fitted best to a rectangular hyperbola (y = x/(2.19 + 0.0015x), r = 0.94). Oleic acid's rate of absorption increased as the hydrogen ion and sodium taurocholate concentrations were increased or as the thickness and resistance of the unstirred water layer were diminished or following the addition of lysolecithin. The additions of the artificial detergent Tween-80, or lecithin and linoleic, linolenic and arachidonic acids to the perfusate decreased oleic acid's rate of absorption. It was concluded that oleic acid absorption in this range of concentrations displays apparent saturation kinetics which are due to unstirred layer effects, limited aqueous solubility of oleic acid and possible saturation of cytosol fatty acid binding proteins. Factors which increase oleic acid's protonated concentration or diminish the unstirred layer resistance, enhance its absorption rate, while factors which enhance its micellar solubility or interfere with its transfer out of the cell membrane decrease its overall rate of absorption.

Animals↗
PubMed1990

The effect of ferrous sulfate and pH on L-dopa absorption.

Ferrous sulfate decreases L-dopa bioavailability in humans probably as a result of binding of L-dopa by iron in the gastrointestinal tract. This study was conducted to determine if iron by binding L-dopa decreases L-dopa absorption and to investigate the effect of different pH buffers on intestinal absorption of L-dopa in the presence and absence of ferrous sulfate. A rat model developed to examine drug absorption was used. Control animals had buffered [14C]L-dopa solutions injected into two in vivo closed segments of intestine; a 5-cm duodenal and a 5-cm proximal jejunal segment. These studies were conducted using solutions buffered at pH 5.5, 6.5, 7.5, and 8.5. An identical procedure was followed for experimental animals except ferrous sulfate was injected with the buffered L-dopa solutions. Ferrous sulfate resulted in a reduction in L-dopa absorption in the buffers at all pHs in both the duodenum and jejunum. The average reduction in L-dopa absorption in the presence of iron was 22.6% in the duodenum and 23.9% in the jejunum. There was a tendency for ferrous sulfate to cause a greater reduction in L-dopa absorption as the buffer pH increased. There was also a decrease in L-dopa absorption in the higher pH buffers in the absence of iron. Despite this latter result, in the jejunum there was an increase in the percent reduction in L-dopa absorption associated with ferrous sulfate as pH increased. Although this tendency was not as consistent in the duodenum as the jejunum, the combined results are compatible with the chemical model of increased L-dopa--iron binding as pH increases.

Animals↗
PubMed1989

Membrane site of action of CO2 on colonic sodium absorption.

Increases in ambient CO2 tension increase colonic sodium absorption by increasing mucosal to serosal sodium flux. We examined the membrane site of CO2 action by utilizing the polyene antibiotic nystatin to create aqueous pores in the apical membrane. Under these conditions, the basolateral rather than the apical membrane is rate limiting for sodium absorption. Pairs of stripped rat distal colonic segments were mounted in modified Ussing chambers in a Ringer-HCO3 solution gassed with either 3% CO2-97% O2 or 11% CO2-89% O2. Mucosal-to-serosal 22Na and 36Cl fluxes were measured under short-circuited conditions, and ouabain-sensitive absorption was calculated before and after the addition of mucosal nystatin 300 U/ml. Ouabain-sensitive sodium absorption was fivefold greater at 11% CO2 than at 3% CO2 before nystatin addition. Nystatin increased short-circuit current (Isc), transcolonic conductance (Gt) and ouabain-sensitive sodium absorption at 3% CO2 but only increased Isc and Gt at 11% CO2. The levels of sodium absorption at 3% and 11% CO2 after nystatin were equal and identical to the level measured at 11% CO2 in the absence of nystatin. Ouabain-sensitive chloride absorption was similar at 3% and 11% CO2 in the absence of nystatin and was not affected by nystatin addition. These findings suggest that ambient CO2 tension affects colonic sodium absorption by a selective action at the apical membrane.

Animals↗
PubMed1998

Nerve growth factor regulates HCO3- absorption in thick ascending limb: modifying effects of vasopressin.

Growth factors stimulate Na+/H+ exchange activity in many cell types but their effects on acid secretion via this mechanism in renal tubules are poorly understood. We examined the regulation of HCO3- absorption by nerve growth factor (NGF) in the rat medullary thick ascending limb (MTAL), which absorbs HCO3- via apical membrane Na+/H+ exchange. MTAL were perfused in vitro with 25 mM HCO3- solutions (pH 7.4; 290 mosmol/kgH2O). Addition of 0.7 nM NGF to the bath decreased HCO3- absorption from 13.1 +/- 1.1 to 9.6 +/- 0.8 pmol.min-1.mm-1 (P < 0.001). In contrast, with 10(-10) M arginine vasopressin (AVP) in the bath, addition of NGF to the bath increased HCO3- absorption from 8.0 +/- 1.6 to 12.5 +/- 1.3 pmol.min-1.mm-1 (P < 0.01). Both effects of NGF were blocked by genistein, consistent with the involvement of tyrosine kinase pathways. However, the AVP-dependent stimulation required activation of protein kinase C (PKC), whereas the inhibition was PKC independent, indicating that the NGF-induced signaling pathways leading to inhibition and stimulation of HCO3- absorption are distinct. Hypertonicity blocked the inhibition but not the AVP-dependent stimulation, suggesting that hypertonicity and NGF may inhibit HCO3- absorption via a common mechanism. These data demonstrate that NGF inhibits HCO3- absorption in the MTAL under basal conditions but stimulates HCO3- absorption in the presence of AVP, effects that are mediated through distinct signal transduction pathways. They also show that AVP is a critical determinant of the response of the MTAL to growth factor stimulation and suggest that NGF can either inhibit or stimulate apical Na+/H+ exchange activity depending on its interactions with other regulatory factors. Locally produced growth factors such as NGF may play a role in regulating renal tubule HCO3- absorption.

Absorption↗
PubMed2005

Role of intestinal sterol transporters Abcg5, Abcg8, and Npc1l1 in cholesterol absorption in mice: gender and age effects.

Recent studies have indicated that intestinal cholesterol absorption is a multistep process, which is regulated by multiple genes at the enterocyte level. However, the molecular mechanisms whereby there are gender differences in intestinal cholesterol absorption efficiency and the efficiency of cholesterol absorption increases with age have not yet been fully understood. To explore whether aging increases cholesterol absorption via intestinal sterol transporters, we studied the higher cholesterol-absorbing C57L/J vs. the lower cholesterol-absorbing AKR/J mice at 8 (young adult), 36 (older adult), and 50 (aged) wk of age. To test the hypothesis that estrogen receptor (ER )alpha plays an important regulatory role in cholesterol absorption, we investigated the gonadectomized mice of both genders treated with 17beta-estradiol-releasing pellets at 0, 3, or 6 mug/day and antiestrogenic ICI 182,780 at 125 microg/day. We found that hepatic outputs of biliary cholesterol were significantly increased with age and in response to high levels of estrogen. Aging significantly enhances cholesterol absorption by suppressing expression of the jejunal and ileal sterol efflux transporters [ATP-binding cassette (Abc)g5 and Abcg8] and upregulating expression of the putative duodenal and jejunal sterol influx transporter Npc1l1. Estrogen significantly augmented cholesterol absorption mostly due to an upregulated expression of intestinal Npc1l1, Abcg5, and Abcg8 via the intestinal ERalpha pathway, which can be fully abolished by the antagonist. We conclude that ERalpha activated by estrogen and aging enhances cholesterol absorption by increasing biliary lipid output and mediating intestinal sterol transporters favoring influx of intraluminal cholesterol molecules across the apical membrane of the enterocyte.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2003

Copper deficiency increases iron absorption in the rat.

Release of iron from enterocytes and hepatocytes is thought to require the copper-dependent ferroxidase activity of hephaestin (Hp) and ceruloplasmin (Cp), respectively. In swine, copper deficiency (CD) impairs iron absorption, but whether this occurs in rats is unclear. By feeding a diet deficient in copper, CD was produced, as evidenced by the loss of copper-dependent plasma ferroxidase I activity, and in enterocytes, CD reduced copper levels and copper-dependent oxidase activity. Hematocrit was reduced, and liver iron was doubled. CD reduced duodenal mucosal iron and ferritin, whereas CD increased iron absorption. Duodenal mucosal DMT1-IRE and ferroportin1 expression remained constant with CD. When absorption in CD rats was compared with that seen normally and in iron-deficient anemic animals, strong correlations were found among mucosal iron, ferritin, and iron absorption, suggesting that the level of iron absorption was appropriate given that the erythroid and stores stimulators of iron absorption are opposed in CD. Because CD reduced the activity of Cp, as evidenced by copper-dependent plasma ferroxidase I activity and hepatocyte iron accumulation, but iron absorption increased, it is unlikely that the ferroxidase activity of Hp is important and suggests another function for this protein in the export of iron from the enterocyte during iron absorption. Also, the copper-dependent ferroxidase activity of Cp does not appear important for iron efflux from macrophages, because Kupffer cells of the liver and nonheme iron levels of the spleen were normal during copper deficiency, suggesting another role for Cp in these cells.

Absorption↗
PubMed1984

Effect of vitamin D3 on duodenal calcium absorption in vivo during early development.

The effect of 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] and vitamin D deficiency on duodenal calcium absorption in suckling and weaned rats was determined by an in situ loop technique. In vitamin D-replete (+D) rats, the linear, or nonsaturable, component of calcium absorption was very efficient in 14-day-old pups and decreased with age until 35 days. The saturable component, which was undetectable in 14-day-old pups, became detectable by 18 days of age and increased until 26 days of age. Calcium absorption was not reduced in vitamin D-deficient (-D) 14-day-old pups as compared with +D pups. A high dose of 1,25(OH)2D3 increased the plasma calcium level of +D suckling rats but had no effect on calcium absorption even with milk present in the loop. Weaned -D rats had a reduced saturable component of absorption (P less than 0.01) compared with +D rats. A high dose of 1,25(OH)2D3 significantly increased calcium absorption and plasma calcium levels of -D rats. Our results indicate that during suckling calcium absorption occurs by a process that is insensitive to vitamin D. After weaning both saturable and nonsaturable processes appear to contribute to calcium absorption, and the saturable component can be influenced by vitamin D status or a high dose of 1,25(OH)2D3.

Aging↗
PubMed1984

Modulation of jejunal ion and water absorption by endogenous angiotensin after dehydration.

In the pentobarbital sodium-anesthetized rat, dehydration for 24 h increased ion and water absorption from the jejunum. Dehydration also elevated plasma concentrations of angiotensin peptides and plasma renin activity but did not significantly alter plasma aldosterone concentrations. Infusion of tyramine, norepinephrine, and angiotensin II (AII) also stimulated jejunal absorption in a manner similar to dehydration. The elevation of jejunal absorption in response to dehydration is totally inhibited by the converting enzyme inhibitor captopril and the angiotensin receptor antagonist [lle7]AIII. Thus, increased jejunal absorption following dehydration is mediated by the renin-angiotensin system and is not secondary to either aldosterone or to antidiuretic hormone release. Further experiments demonstrated that the increase in jejunal absorption in response to dehydration was unaffected by propranolol but was totally abolished by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII stimulates jejunal absorption by enhancing transepithelial transport processes and/or by altering the balance of Starling forces governing fluid absorption across enteric capillaries. Angiotensin thus appears to be a physiologically important mediator of jejunal absorption in states characterized by extracellular volume depletion.

Absorption↗
PubMed1984

Effect of arterial carbon dioxide tension on amiloride-sensitive sodium absorption in the colon.

To examine the nature of the electroneutral sodium chloride absorptive process affected by arterial carbon dioxide tension (PCO2), we measured the effects of amiloride on colonic sodium absorption at concentrations (0.75 mM) known to inhibit cell membrane sodium-hydrogen ion exchange. During sequential in situ perfusions of distal colon with amiloride-free and amiloride-containing solutions, water and electrolyte transport was measured in anesthetized, mechanically ventilated rats during normocapnia, respiratory alkalosis, or respiratory acidosis. During amiloride-free perfusions, alkalosis decreased and acidosis increased net water, sodium, and chloride absorption without changing the transmural potential difference. Perfusion of amiloride (0.75 mM) caused a similar fractional decrease in net sodium absorption in alkalotic (-53.3 +/- 10.2%), normocapnic (-46.3 +/- 6.5%), and acidotic rats (-57.2 +/- 5.2%). Net water (-43%) and chloride absorption also exhibited equivalent fractional reductions in the three acid-base states during amiloride perfusion, although net chloride absorption was reduced only about 20%. These results suggest that the specific colonic sodium absorptive process affected by arterial PCO2 is an amiloride-sensitive, sodium-hydrogen ion exchange process. Arterial PCO2 probably also affects a mucosal chloride-bicarbonate exchange process that results in its overall effect on electroneutral sodium chloride absorption by the distal colon.

Acidosis, Respiratory↗
PubMed1990

Meal-stimulated absorption of water and electrolytes in canine jejunum.

After a meal, the absorption of water and electrolytes from the jejunal lumen increases. This meal-induced jejunal absorption occurs in jejunal segments out of normal gastrointestinal continuity. The experimental model used 25-cm proximal jejunal Thiry-Vella loops in awake dogs (n = 72 observations) to evaluate the mechanisms involved in meal-induced jejunal absorption, seeking to define the source or sources of the proabsorptive signal. Specifically, we evaluated the jejunal absorptive response to a standard meal, a standard meal plus cholinergic blockage using atropine, a sham-fed meal, a gavage-fed meal, and gastric distension with balloon and gavage water. Both the standard meal and the gavage-fed meal induced a prompt, sustained, and significant (P less than 0.0001) increase in the absorption of H2O, Na+, and Cl-. Atropine significantly reduced the magnitude of the postmeal absorptive response (P less than 0.05) compared with the standard meal alone. The sham-fed meal, gastric balloon distension, and gavage water did not alter jejunal absorption. Vagal nerve integrity after cervical esophageal manipulation was verified by gastric acid output and gastrin response to stimuli. These data support a role for cholinergic modulation of meal-stimulated jejunal absorption via a cephalic-phase-independent and gastric-distension-independent mechanism.

Animals↗
PubMed1993

Effect of intracellular acidification on colonic NaCl absorption.

CO2 stimulates Na+ and Cl- absorption in rat distal colon. This is most likely due to intracellular generation of H+ and HCO3- and stimulation of apical Na(+)-H+ and Cl(-)-HCO3- exchangers. We examined whether intracellular acidification by means other than CO2 would also stimulate Na+ absorption. Stripped segments of distal colon from male Sprague-Dawley rats were studied under short-circuit conditions in Ussing chambers. Identically prepared tissues were used for intracellular pH (pHi) measurements with the pH-sensitive dye 2',7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. When the Ringer PCO2 was increased from 20 to 34 mmHg, pHi decreased from 7.50 +/- 0.04 to 7.35 +/- 0.04 and net Na absorption increased from 2.4 +/- 0.7 to 3.7 +/- 0.7 mu eq.cm-2 x h-1. A similar degree of intracellular acidification was obtained with 2.6 microM nigericin, but no stimulation of Na+ absorption was seen. When Ringer-HCO3- concentration was reduced from 39 to 11 mM at constant PCO2 = 35 mmHg, pHi decreased from 7.55 +/- 0.02 to 7.11 +/- 0.02 with no effect on net Na+ absorption. A similar reduction in pHi in a CO2-HCO3(-)-free, N-2-hydroxyethylpiperazine-N'-2-ethanesulfonic acid-buffered Ringer also did not stimulate Na+ absorption. Methazolamide had no effect on steady-state pHi at any given PCO2 but caused marked reductions in net Na+ absorption (9.6 +/- 2.4 to 5.2 +/- 1.2 mu eq.cm-2 x h-1 at PCO2 = 70 mmHg). We conclude that Na+ absorption in rat distal colon is not stimulated by intracellular acidification per se but rather has an absolute requirement for CO2 and carbonic anhydrase activity.

Animals↗