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PubMed1978

A membrane model of the human oral mucosa as derived from buccal absorption performance and physicochemical properties of the beta-blocking drugs atenolol and propranolol.

The buccal absorption characteristics and physicochemical properties of the beta-adrenoceptor blocking agents propranolol and atenolol have been investigated to evaluate their permeation properties across biological lipid membranes. The dissociation constants, solubilities of free base, and n-heptane partition coefficients show that propranolol in its unionized form is much more lipophilic than atenolol, both drugs being bases with a similar pKa. Buccal absorption was studied under conditions of varying drug concentration, contact time, and pH, and controlled through the use of a non-absorbable marker. The absorption findings are in general agreement with the pH-partition theory. A new compartmental diffusional model that includes membrane storage and a hypothetical "aqueous pH-buffering surfaces system" allowed a more exhaustive interpretation to be made. A method for the estimation of the intrinsic pH and buffer capacity of the postulated surface system from drug pH-absorption data and partition coefficients alone is described. With human oral mucosa the intrinsic pH was near 6.7, and the buffering capacity of the system (expressed as the ratio deltapH/deltapH eff) about 2.86. The method was validated using published absorption data from the rat small intestine. Absorption of unionized drug through pores is shown to be negligible in the buccal absorption situation. The time course of absorption suggests membrane storage of lipophilic compounds; the in vivo partition coefficient of unionized propranolol relative to the mucous membrane could be calculated for the peusdo-steady state of absorption, i.e. the partition equilibrium between mouth content and membrane, to be approximately 776; this value is of the same order as the in vitro partition coefficient for the erythrocyte/plasma system. The lipid biophase of the buccal membrane is estimated semiquantitatively to be of intermediate polarity (epsilon = 3-4).

Absorption↗
PubMed2006

Intestinal phosphate absorption and the effect of vitamin D: a comparison of rats with mice.

Previously, it was thought that intestinal phosphate transport occurred exclusively in the proximal small intestine of rodents and humans. However, a recent study has demonstrated that the ileum of mice contributes significantly to the absorption of dietary phosphate, but it is not known whether this region is also an important site of phosphate absorption in the rat. In the present study, we have investigated the mRNA and protein levels of the sodium-phosphate cotransporter, NaPi-IIb, in three regions of rat and mouse small intestine, and related its expression levels to the rate of net phosphate absorption, as measured using the in situ intestinal loop technique. 1,25-Dihydroxyvitamin D3 is an important physiological regulator of intestinal phosphate absorption that increases phosphate transport in both the duodenum and jejunum of the rat. Based on the recently proposed regional profile of phosphate absorption along the mouse small intestine, we have re-evaluated the effects of 1,25-dihydroxyvitamin D3 using three distinct regions of the mouse and rat small intestine. Our studies have revealed important differences in the intestinal handling of phosphate between mice and rats. In mice, maximal phosphate absorption occurs in the ileum, which is paralleled by the highest expression levels of NaPi-IIb mRNA and protein. In contrast, in rats maximal absorption occurs in the duodenum with very little absorption occurring in the ileum, which is similar to the pattern reported in humans. However, in both rodent species only the jejunum shows an increase in phosphate absorption in response to treatment with 1,25-dihydroxyvitamin D3.

Animals↗
PubMed1978

Effects of vasoactive intestinal polypeptide on intestinal absorption and blood flow.

1. Intestinal absorption and blood flow in anaesthetized dogs was determined after I.V. infusion of vasoactive intestinal polypeptide (VIP) (1.75-175 ng/min) to determine the contribution of the cardiovascular changes to transport. 2. 22Na and 3H2O were utilized to determine the unidirectional fluxes of Na and H2O from saline perfused through the ileal lumen and the clearances of 3H2O were used to determine total and absorptive site blood flow. 3. Net Na and H2O absorption were reversed to secretion by VIP at 175 ng/min due to a significant decrease in unidirectional absorptive fluxes and smaller increases in secretory fluxes. 4. Arterial pressure and absorptive site blood flow were reduced in proportion to the changes in Na and H2O fluxes. 5. Total and absorptive site blood flow decreased and the blood flow resistances increased. 6. Prior treatment with guanethidine to suppress sympathetic effects did not greatly affect the responses to VIP. Prior treatment with atropine to suppress cholinergic effects inhibited most of the effects of VIP. 7. Absorptive site blood flow was linearly related to absorptive fluxes of Na and H2O but with different slopes for results from atropinized dogs as compared to those from dogs given VIP alone or VIP plus guanethidine. 8. It was concluded that VIP reduces gut absorption through a generalized cardiovascular effect and also through a mechanism which depends on the release of ACh by the gut.

Animals↗
PubMed1987

Fluid absorption by rat lung in situ: pathways for sodium entry in the luminal membrane of alveolar epithelium.

1. The purpose of the investigation was to characterize the luminal membrane and the paracellular pathway of rat lung alveolar epithelium. Experiments were performed on lungs in situ instilled with isotonic, buffered Ringer solution and perfused with blood from a donor rat using cross-circulation technique. 2. The rate of active Na+ transport was 4.4 pmol/(cm2s). The fluid absorption was 156 nl/s, and was unaffected by the presence of protein in the instillate (166 nl/s). In the absence of Na+, fluid absorption was zero. Amiloride (10(-3) M) reduced fluid absorption by 60%. Amiloride, combined with absence of D-glucose, arrested fluid absorption completely. Phloridzin at the luminal side reduced fluid absorption whilst phloretin had no effect. Amiloride together with phloridzin (10(-3) M) also arrested absorption. Thus, there are two entry systems for Na+ in the luminal membrane: Na+ channels and a Na+-D-glucose symport. These results show that alveolar fluid absorption is due to cellular activity. 3. Substitution of Cl- with gluconate not only stopped fluid absorption, but led to slight reversal of net fluid movement. 4. Passive unidirectional flux of Na+, determined with 22Na+, was 9.9 pmol/(cm2s) and that of Cl-, determined with 36Cl-, was 12.4 pmol/(cm2s). These fluxes were based on an assumed alveolar surface area of 5000 cm2. Transference numbers calculated from these figures are close to those in free solution, suggesting a neutral or weakly charged intercellular junctional pathway. The D-mannitol permeability in the paracellular pathway was 1.7 X 10(-8) cm/s. 5. It is a consequence of the proposed mechanism for fluid absorption that it becomes inoperative if the normally high reflexion coefficients for Na+ and Cl- are lowered in pathological states. In such conditions pulmonary oedema may develop depending on the net balance of passive mechanical and colloid-osmotic forces. 6. An explanation of the reversal of fluid transport at the time of birth is presented.

Absorption↗
PubMed1997

L-arginine in low concentration improves rat intestinal water and sodium absorption from oral rehydration solutions.

BACKGROUND: The nitric oxide (NO) precursor L-arginine has been shown to produce variable effects on intestinal absorptive function, including ion transport. AIMS: To determine whether there is an optimal concentration of L-arginine, promoting proabsorptive effects from oral rehydration solutions (ORS) with 90 or 60 mM sodium. SUBJECTS AND METHODS: In vivo perfusion of rat jejunum with determination of net water absorption, unidirectional fluid exchanges, sodium and calcium transport, and glucose absorption. RESULTS: L-Arginine (1 mM) added to the 90 mM sodium ORS increased intestinal absorption of both sodium and water. Higher concentrations of L-arginine (2 to 10 mM) lacked this stimulatory effect. At 20 mM, L-arginine decreased sodium absorption below baseline. With a 60 mM sodium ORS, 2 mM L-arginine had a maximal fluid and electrolyte proabsorptive effect. At 20 mM L-arginine, net water absorption was indistinguishable from that obtained in the absence of L-arginine, and lower than with 2 mM L-arginine. Sodium absorption remained raised above baseline in perfusions with 10 and 20 mM L-arginine. Morphologically, villi from perfusions with increased absorption showed a large expansion of intercellular and lamina propria intercellular spaces. CONCLUSIONS: Low concentrations of L-arginine seem to stimulate water and electrolyte absorption by the small intestine. This effect is consistent with NO induced vasodilation, may be vaso-constrictive and thereby reverse fluid and electrolyte transport.

Animals↗
PubMed2003

Apical NHE isoforms differentially regulate butyrate-stimulated Na absorption in rat distal colon.

Bicarbonate and butyrate stimulate electroneutral Na absorption via apical membrane Na-H exchange (NHE) in rat distal colon. cAMP downregulates NHE-3 isoform and inhibits HCO3-dependent, but not butyrate-dependent, Na absorption. This study sought to determine whether 1) the apical membrane NHE-2 and NHE-3 isoforms differentially mediated HCO3- and butyrate-dependent Na absorption, and 2) cAMP had different effects on NHE-2 and NHE-3 isoforms. The effect of specific inhibitors of NHE-2 and NHE-3 isoforms (50 microM HOE 694 and 2 microM S3226, respectively) on unidirectional 22Na transepithelial fluxes performed across isolated mucosa from rat distal colon under voltage-clamp conditions was examined. HCO3 stimulation of Na absorption was inhibited by EIPA, a nonspecific inhibitor of all NHE isoforms, by S3226 and dibutyryl cAMP but not by HOE 694. In contrast, butyrate stimulation of Na absorption was not altered by dibutyryl cAMP and was not inhibited by HOE 694 in the absence of dibutyryl cAMP, but in the presence of dibutyryl cAMP was HOE694 sensitive. In contrast, S3226 inhibited butyrate-stimulated Na absorption in the absence of dibutyryl cAMP, but not in its presence. We conclude that 1) HCO3-stimulated Na absorption is mediated solely by NHE-3 isoform, whereas butyrate-stimulated Na absorption is mediated by either NHE-3 or NHE-2 isoform, and 2) dibutyryl cAMP selectively inhibits NHE-3 isoform but stimulates NHE-2 isoform. Dibutyryl cAMP does not inhibit butyrate-stimulated Na absorption as a result of its differential effects on NHE-2 and NHE-3 isoforms.

Animals↗
PubMed1984

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

In the pentobarbital sodium-anesthetized rat, hemorrhage of blood equivalent to 1% body weight (18.4% blood volume) increases plasma renin activity and plasma aldosterone concentration and also markedly elevates jejunal ion and water absorption. Infusion of angiotensin II (AII) also stimulates jejunal absorption, and in a manner similar to hemorrhage. The elevation of jejunal absorption in response to hemorrhage is not affected by removal of the adrenals but is totally inhibited by the converting enzyme inhibitor captopril and by bilateral nephrectomy. Thus, increased jejunal absorption following hemorrhage is mediated by the renin-angiotensin system and is not secondary to aldosterone release. Further experiments demonstrated that norepinephrine released from enteric sympathetic nerves controls jejunal absorption through activation of alpha-adrenergic receptors. The stimulation of jejunal absorption by tyramine was unaffected by propranolol but was totally abolished by phentolamine and by peripheral sympathectomy was 6-hydroxydopamine (intact adrenal medulla). The increase in jejunal absorption in response to hemorrhage also was unaffected by propranolol but was inhibited totally by phentolamine, prazosin, and peripheral sympathectomy. It is proposed that AII generated by hemorrhage facilitates norepinephrine release from enteric sympathetic nerves. The norepinephrine released by AII stimulates jejunal absorption by enhancing transepithelial transport processes or by altering the balance of Starling forces governing fluid absorption across enteric capillaries.

Adrenalectomy↗
PubMed1987

Mechanisms of enhanced canine enteric absorption with intestinal pacing.

Electrical pacing enhances absorption from the canine small bowel, but the mechanism of this effect is unknown. To explore the mechanism, conscious dogs with two Vella loops, a proximal jejunal and a distal ileal, each 50 cm long, were studied. Pacing the jejunal loop with 15-18 pulses/min entrained the pacesetter potentials of the jejunal loop and increased water, sodium, and glucose absorption from the jejunal loop. Jejunal pacing also increased water absorption from the unpaced, ileal loop. Conversely, ileal pacing did not entrain the ileal loop or enhance absorption from the ileal loop. However, it did enhance water absorption in the unpaced jejunal loop. After alpha-blockade with phentolamine or celiac and superior mesenteric ganglionectomy, jejunal pacing did not increase jejunal or ileal absorption. In contrast, after beta-blockade with propranolol, pacing still enhanced jejunal absorption in three out of four dogs. Vagotomy alone enhanced jejunal but not ileal absorption, but the enhancement was not further increased by pacing. In conclusion, electrical pacing of the small bowel elicited a local and distant increase in net water absorption; the effect was mediated in part by an alpha-adrenergic mechanism.

Animals↗
PubMed1994

Brush-border tyrosine phosphorylation stimulates ileal neutral NaCl absorption and brush-border Na(+)-H+ exchange.

The drug genistein, a tyrosine (Tyr) kinase inhibitor, was used to define a role for Tyr phosphorylation in regulation of basal and stimulated neutral NaCl absorption in rabbit ileum. Brush-border vesicles contain Tyr-phosphorylated peptides. Genistein freeze-thawed into the vesicles caused a concentration-dependent inhibition of at least three peptides with M(r) 111,000, 83,000, and 80,000. Studied with the Ussing chamber-voltage clamp technique, genistein added to the ileal mucosal surface inhibited neutral NaCl absorption. Direct addition of genistein to brush-border vesicles made from ileal villus cells inhibited brush-border Na(+)-H+ exchange but not D-glucose-stimulated Na+ uptake. These effects were not duplicated by genistin, a drug with similar structure to genistein but lacking Tyr kinase inhibiting properties. Serosal but not mucosal epidermal growth factor (EGF) stimulated NaCl absorption. Mucosal genistein but not genistin also altered second-messenger regulation of neutral NaCl absorption, inhibiting the effect of Ca2+ ionophore A-23187 and of serosal EGF but not affecting the transport changes caused by 8-bromoadenosine 3',5'-cyclic monophosphate (8-BrcAMP). In contrast, the Cl secretory effects indicated by the increase in short-circuit current for all three agents, A-23187, EGF, and 8-BrcAMP, were inhibited by mucosal genistein. These results suggest that 1) a Tyr kinase is involved in basally stimulating ileal neutral NaCl absorption and brush-border Na(+)-H+ exchange; 2) EGF stimulates NaCl absorption by an effect exerted from the serosal surface, but the effect also involves a brush-border Tyr kinase; 3) brush-border Tyr kinase is involved in the ability of Ca2+ ionophore A-23187 to inhibit neutral NaCl absorption but is not involved in the transport effects of cAMP. This study suggests that Tyr kinase(s) acting over short time periods is involved in stimulation of neutral NaCl absorption and brush-border Na(+)-H+ exchange and also in Ca(2+)-induced inhibition of NaCl absorption. These studies represent the first example of a brush-border Tyr kinase being involved in short-term signal transduction in intestinal epithelial cells.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1976

Vitamin K2 absorption by rat everted small intestinal sacs.

Small intestinal absorption of vitamin K2 was investigated in vitro. Experiments with increasing concentrations of the vitamin up to 900 nM revealed linerity between the concentration and the rate of absorption (r = 0.99). Addition of metabolic uncouplers and inhibitors such as 2,4-dinitrophenol, sodium azide, and potassium cyanide did not decrease the rate of absorption of the vitamin (P less than 0.05). Absorption rate of the vitamin increased when taurocholate was replaced by a nonionic detergent, Pluronic F-68. The addition of butyric and octanoic acids to the incubation solution caused an increase in the absorption rate of vitamin K2. No change in the absorption of the vitamin occurred in the presence of oleic and linoleic acid. Addition to vitamins K1 and K3 to the incubation solution did not change the rate of vitamin K2 absorption. These findings suggest that vitamin K2 is absorbed by the small bowel by a passive noncarrier-mediated diffusion process. The rate of diffusion varied when the lipid and bile salt composition of the incubation solution was modified. Distal intestinal absorption of vitamin K from bacterial sources coupled with colonic absorption of the vitamin may be the major constant source of vitamin K in mammals.

Animals↗
PubMed1976

Effects of diabetes on intestinal magnesium absorption in the rat.

Control and streptozotocin-diabetic rats were studied at 5, 12, and 32 days after induction of diabetes. Magnesium absorption was measured by in situ perfusion of duodenum and ileum. At 5 days, duodenal mucosal growth is similar in controls and diabetics. At 12 days, mucosal growth is 50% greater in diabetics, and at 32 days, 100% greater. Ileal mucosal growth followed the same pattern but was half that of duodenum. Therefore, absorption data were expressed per centimeter segment length to define absorptive capacity of the segment and per gram dry weight of mucosa to define absorptive specific activity. Mean absorptive specific activity was lower in diabetics than controls at all time intervals. The difference was significant only for duodenum of diabetics at 32 days, when magnesium absorption declined to half that of controls. In contrast, absorptive capacity for both segments remained the same in both groups, attributable to the greater mucosal growth in diabetics. These findings for magnesium contrast with effects of diabetes on calcium transport: specific absorption and segment absorptive capacity are depressed in diabetics at both 5 and 11 days. Thus, although transport of magnesium and calcium usually tend to change in parallel in diabetes, transport of magnesium is depressed later and to a lesser degree than calcium, and segment transport capacity is maintained. The findings suggest differences in mechanism of regulation of magnesium and calcium transport.

Animals↗
PubMed1979

Physiological basis for absorptive and renal hypercalciurias.

Idiopathic hypercalciuria constitutes two major variants-absorptive hypercalciuria, characterized by a primary intestinal hyperabsorption of calcium, and renal hypercalciuria, in which renal tubular reabsorption of calcium is primarily impaired. The two forms of hypercalciuria may be distinguished from each other, since a) parathyroid function is stimualted in renal hypercalciuria, but normal or suppressed in absorptive hypercalciuria, b) the renal leak of calcium is present in renal hypercalciuria, but not in absorptive hypercalciuria, c) intestinal calcium absorption is probably increased primarily in absorptive hypercalciuria, and secondarily in renal hypercalciuria (from parathyroid hormone excess), d) the increased calcium absorption in renal hypercalciuria probably results from the parathyroid hormone-dependent stimulation of 1,25-dihydroxyvitamin D synthesis, whereas that in absorptive hypercalciuria may be vitamin D-independent, e) the response of the two conditions to certain treatments is unique, and f) the sequelae of parathyroid hormone excess, such as low bone density and negative calcium balance, may be present in renal hypercalciuria, but not in absorptive hypercalciuria. These findings provide a physiological basis for the consideration of absorptive and renal hypercalciurias as distinct and separate entities.

Benzothiadiazines↗
PubMed1988

Active absorption of NH4+ by rat medullary thick ascending limb: inhibition by potassium.

These experiments were designed to determine the relative contributions of active NH4+ transport and voltage-driven NH4+ diffusion to direct NH4+ absorption by the medullary thick ascending limb of the rat. Medullary thick ascending limbs were perfused in vitro with solutions containing 25 mM HCO3 and 4 mM total ammonia. Under steady-state conditions, the lumen-positive transepithelial voltage (VT) was not sufficient to account for the observed decrease in lumen NH4+ concentration, consistent with active absorption of NH4+. Flux calculations based on VT and measured NH4+ permeability (6 x 10(-5) cm/s) indicate that the majority (at least 65%) of total ammonia absorption is due to active transport of NH4+. The remainder of NH4+ absorption can be accounted for by voltage-driven diffusion. Increasing the potassium concentration from 4 to 24 mM in perfusate and bath markedly inhibited total ammonia absorption but did not affect VT, NH4+ permeability, or HCO3 absorption. These results are consistent with inhibition of the active component of NH4+ absorption by potassium. The active NH4+ absorption is likely mediated by cotransport of Na+, NH4+, and Cl- across the apical cell membrane. Inhibition of active NH4+ absorption by an increase in potassium concentration may be due, in part, to competition between NH4+ and K+ for a common binding site on the Na+ -K+ -2Cl- cotransport system.

Absorption↗
PubMed2001

Role of basolateral carbonic anhydrase in proximal tubular fluid and bicarbonate absorption.

Membrane-bound carbonic anhydrase (CA) is critical to renal acidification. The role of CA activity on the basolateral membrane of the proximal tubule has not been defined clearly. To investigate this issue in microperfused rabbit proximal straight tubules in vitro, we measured fluid and HCO(3)(-) absorption and cell pH before and after the extracellular CA inhibitor p-fluorobenzyl-aminobenzolamide was applied in the bath to inhibit only basolateral CA. This inhibitor was 1% as permeant as acetazolamide. Neutral dextran (2 g/dl, molecular mass 70,000) was used as a colloid to support fluid absorption because albumin could affect CO(2) diffusion and rheogenic HCO(3)(-) efflux. Indeed, dextran in the bath stimulated fluid absorption by 55% over albumin. Basolateral CA inhibition reduced fluid absorption ( approximately 30%) and markedly decreased HCO(3)(-) absorption ( approximately 60%), both reversible when CA was added to the bathing solution. In the presence of luminal CA inhibition, which reduced fluid ( approximately 16%) and HCO(3)(-) ( approximately 66%) absorption, inhibition of basolateral CA further decreased the absorption of fluid (to 74% of baseline) and HCO(3)(-) (to 22% of baseline). CA inhibition also alkalinized cell pH by approximately 0.2 units, suggesting the presence of an alkaline disequilibrium pH in the interspace, which would secondarily block HCO(3)(-) exit from the cell and thereby decrease luminal proton secretion (HCO(3)(-) absorption). These data clearly indicate that basolateral CA has an important role in mediating fluid and especially HCO(3)(-) absorption in the proximal straight tubule.

Absorption↗
PubMed1994

Folate absorption in Crohn's disease.

An oral folate absorption test was performed in 100 consecutive patients with Crohn's disease (CD) and 20 healthy individuals to investigate the frequency of abnormal folate absorption in regard to the site of the disease and to investigate the possibility of defining a subgroup of patients requiring parenteral folate supplementation. The described oral folate absorption test can be performed quickly on an outpatient basis and is capable of distinguishing patients with altered folate absorption from those with normal folate absorption. In 25 patients, abnormal folate absorption was detected. 16 patients showed impaired folate absorption as indicated by a marked but insufficient increase in serum folate levels after oral folate intake, whereas no increase of the serum folate levels was detected in the remaining 9 patients. Abnormal folate absorption was not correlated with disease extent or activity. In patients with only impaired folate absorption, it might be sufficient to increase dietary intake of folates. In the remaining patients with no measurable increase of serum folate levels after oral folate intake, i.e. about 10% of all patients with CD, parenteral folate supplementation could be considered.

Administration, Oral↗
PubMed1974

Inhibition of ileal water absorption by intraluminal fatty acids. Influence of chain length, hydroxylation, and conjugation of fatty acids.

The influence of fatty acids on ileal absorption of water, electrolytes, glucose, and taurocholate was examined in Thirty-Vella fistulas in five mongrel dogs. Fatty acid absorption also was measured. Segments of terminal ileum were perfused at steady state with isotonic electrolyte solutions containing 11.2 mM glucose, 4.5 mM taurocholate, and 0.1-5.0 mM fatty acid. Three C(18) fatty acids, oleic acid, 10(9)-hydroxystearic acid, and ricinoleic acid, completely inhibited water absorption at 5 mM. Sodium, chloride, and potassium absorptions were inhibited in parallel with absorption of water. Differences between the potencies of C(18) fatty acids were apparent when lesser concentrations were perfused. Dodecanoic and decanoic acids were as effective as C(18) fatty acids at 5 mM but octanoic and hexanoic acids were ineffective. The polar group of C(18) fatty acids was modified by conjugating oleic and ricinoleic acids with taurine. When these compounds and a substituted C(18) fatty acid, p-n-decylbenzenesulfonate, were perfused, water absorption was also inhibited. Short-chain fatty acids (C(3) and C(4)) and their hydroxylated derivatives were ineffective at 5 mM. When water absorption was inhibited, absorption of glucose and taurocholate was decreased. We speculate that the phenomenon of inhibition of water and electrolyte absorption by fatty acids may be relevant to steatorrhea and diarrhea in man.

Animals↗
PubMed1977

Fetal bile salt metabolism. The intestinal absorption of bile salt.

The intestinal absorption of sodium taurocholate was studied in the near-term fetal and neonatal dog. Absorption rates were measured in vivo in isolated loops of fetal jejunum and ileum. Absorption was also measured in vitro in everted sacs and rings of fetal and neonatal jejunum and ileum. The maximal rates of taurocholate absorption observed after instillation of 1 micronmol taurocholate into closed segments of fetal jejunum and ileum with intact blood supply were not significantly different (P less than 0.2), and equalled 0.282+/-0.026 (mean+/-SEM) and 0.347+/-0.051 micronmol/h per 10-cm segment length jejunum and ileum, respectively. Similarly, the rates of absorption from open segments of jejunum and ileum perfused with 0.4 and 1.0 mM taurocholate were nearly identical (0.232+/-0.040 and 0.255+/-0.039, respectively at 0.4 mM, and 0.470+/-0.065 and 0.431+/-0.013, respectively at 1.0 mm) (P greater than 0.2). At perfusate concentrations of 4.0 mM, moreoever, jejunal absorption exceeded ileal absorption (1.490+/-0.140 and 0.922+/-0.200, respectively (P less than 0.05). As expected, concentration of taurocholate by the mucosa was readily demonstrated in adult ileal, but not in adult jejunal everted rings. In contrast, there were no significant differences in mucosal uptake of taurocholate by fetal jejunal and ileal rings. Fetal ileal mucosal concentrations were not significantly above those in the incubation medium after 1-h exposure of the mucosa to 0.003, 0.03, and 0.3 mM taurocholate. Uptake was proportional to incubation medium concentration over the full range of values. This was also true of tissues from 1-wk-old neonates. However, by 2 wk of age, ileal mucosal concentration of taurocholate was evident and adult levels were attained by 5 wk of age. It is concluded that taurocholate is absorbed by the fetal gut and that ileal absorption is no more efficient than jejunal absorption. Although active glucose transport was demonstrable in both jejunum and ileum, it was not possible to demonstrate an ileal mechanism for active transport of taurocholate in the fetus. Active ileal transport was not demonstrable in the newborn until at least 2 wk after birth.

Age Factors↗
PubMed1984

Albumin absorption and catabolism by isolated perfused proximal convoluted tubules of the rabbit.

Overall characteristics and kinetics of tubular absorption of albumin (Alb) were studied in isolated perfused proximal convoluted tubules of the rabbit. The fate of absorbed Alb was determined in tubules perfused with low [Alb]. Alb was labeled with tritium by reductive methylation ( [3H3C]Alb). At [Alb] = 0.03 mg/ml, approximately 80% of the absorbed [3H3C]Alb was released to the peritubular bathing solution as catabolic products. Transcellular transport of intact [3H3C]Alb was negligible. Iodoacetate (IAA, 4 mM) inhibited albumin absorption (JAlb) by greater than 95% and fluid reabsorption (JV) by 55%. At [Alb] = 0.1 mg/ml the absorption rate of a derivatized cationic Alb (pI = 8.4) was fivefold greater (P less than 0.01) than that of anionic Alb. Higher cationic [Alb] had deleterious effects on tubular functions. Overall Alb absorption was of high capacity and low affinity (JmaxAlb = 3.7 ng/min per mm tubule length, apparent Michaelis constant (Km) = 1.2 mg/ml). A low capacity system that saturates at near physiological loads was also detected (JmaxAlb = 0.064 ng/min per mm, apparent Km = 0.031 mg/ml). High [Alb] did not alter the rate of endocytic vesicle formation as determined by the tubular uptake of [14C]inulin. Results show that Alb absorption is a saturable process that is inhibited by high IAA concentrations and is affected by the charge of the protein. Absorbed Alb is hydrolyzed by tubular cells and catabolic products are readily released to the peritubular side. The dual kinetics of Alb absorption may be due to a combination of adsorptive endocytosis (low capacity system) and fluid endocytosis of albumin aggregates (high capacity system). Results indicate that albuminuria occurs much before albumin absorption is saturated. The kinetic characteristics of the process of tubular absorption of albumin helps to explain the concomitance of albuminuria, increased renal catabolic rates of albumin, and renal cell deposition of protein absorption droplets in severe glomerular proteinurias.

Absorption↗