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PubMed1985

Modulatory effects of Freund's adjuvant treatment on mast cell histamine release and homocytotropic antibody synthesis.

The present study examines the influence of Freund's complete adjuvant (FCA) injections on sensitized PVG rats with respect to serum levels of IgE and IgG2 alpha antibodies and total IgE (all assessed by radioimmunoassays) and the capacity of serosal mast cells to release histamine on challenge in vitro with 'immunological' secretagogues (specific antigen, anti-IgE, concanavalin A) or with compound 48/80. The rats were immunized with 10 micrograms ovalbumin (OA); alum, Bordetella pertussis vaccine, or silica gel were employed as adjuvants. Treatment with FCA was performed by single intraperitoneal injections 3, 2, or 1 week(s) before or 1 or 2 weeks after sensitization. Tests were conducted 3 weeks after sensitization. The results show that the effect of FCA treatment varied reproducibly with the adjuvant employed for sensitization and with the timing of the FCA administration. FCA treatment could either increase, fail to affect, or decrease total serum IgE and OA-IgG2 alpha antibody levels as well as serosal mast cell responsiveness, whereas OA-IgE antibody responses were decreased or not affected. Moreover, serum levels of OA-IgE and OA-IgG2 alpha antibodies and total IgE were affected by FCA treatment independently of each other. Finally, serosal mast cell responsiveness to a given secretagogue could be influenced by the FCA treatment apparently independently of that to other secretagogues. A salient finding was that effects of FCA treatment on mast cell responsiveness did not necessarily conform to effects on antibody synthesis. Collectively, these data support the opinion that the mechanisms of action of the IgE-promoting adjuvants employed differ and suggest that the expression of serosal mast cell responsiveness to each examined secretagogue can be regulated separately. They also suggest that the serosal mast cell sensitizing capacity of homocytotropic antibodies may not be adequately quantified by immunochemical methods employing reagents prepared against IgE and IgG2 alpha protein.

Alum Compounds↗
PubMed1967

Ammonia movement in the small intestine: preferential transport by the ileum.

Isolated, surviving sacs of everted small intestine were used to characterize ammonia transport in the golden hamster. Jejunal and ileal sacs incubated aerobically in ammonia-free test solution liberated the same quantity of ammonia as did sacs that were filled and immediately emptied of their contents, indicating no significant evolution of metabolic ammonia. Under aerobic conditions, ileal sacs transferred a solution of high ammonia content from the mucosal surface to the serosal surface against a concentration gradient. This transport was not glucose dependent and exhibited first-order Michaelis-Menten kinetics. Inhibition of absorption occurred with anaerobiosis, 2,4-dinitrophenol, and sodium cyanide. In jejunal segments ammonia was not transported against an adverse chemical gradient. Ileal ammonia absorption was accompanied by bicarbonate secretion and acidification of the serosal solution. Both bicarbonate movement and pH gradients were abolished by inhibitors of ammonia transport. In the jejunum, the absence of ammonia movement occurred in association with minimal bicarbonate secretion and no appreciable change in serosal pH. Despite the creation of hydrogen ion gradients tending to augment or to retard ammonia absorption by nonionic diffusion, ammonia movement was unaffected, i.e., relative acidification of serosal contents did not augment ammonia absorption, and relative alkalinization of serosal fluid caused no inhibition of ammonia transport. In the absence of bicarbonate ion, ammonia transport did not occur. The significance of these findings is discussed with consideration of both ionic and nonionic mechanisms of ammonia movement. It is suggested that ammonia is absorbed in the ileum by active ionic transport.

Ammonia↗
PubMed1985

Chloride secretory mechanism induced by prostaglandin E1 in a colonic epithelial cell line.

Confluent T84 monolayers grown on permeable supports and mounted in a modified Ussing chamber secrete chloride (Cl-) in response to prostaglandin E1. The threshold stimulation was observed at 10(-9) M and a maximal effect at 10(-6) M. Unidirectional flux studies showed an increase in both serosal to mucosal and mucosal to serosal Cl- fluxes with 10(-6) M prostaglandin E1; the increase in serosal to mucosal Cl- flux exceeded the increase in mucosal to serosal flux, resulting in net Cl- secretion. Na+ transport was not affected in either direction and the changes in net Cl- flux correlated well with the changes in short circuit current. To identify the electrolyte transport pathways involved in the Cl- secretory process, the effect of prostaglandin E1 on ion fluxes was tested in the presence of putative inhibitors. Bumetanide was used as an inhibitor for the basolaterally localized Na+,K+,Cl- cotransport system whose existence and bumetanide sensitivity have been verified in earlier studies (Dharmsathaphorn et al. 1984. J. Clin. Invest. 75:462-471). Barium was used as an inhibitor for the K+ efflux pathway on the basolateral membrane whose existence and barium sensitivity were demonstrated in this study by preloading the monolayers with 86Rb+ (as a tracer for K+) and simultaneously measuring 86Rb+ efflux into both serosal and mucosal reservoirs. Both bumetanide and barium inhibited the net chloride secretion induced by prostaglandin E1 suggesting the involvement of the Na+,K+,Cl- cotransport and a K+ efflux pathways on the basolateral membrane in the Cl- secretory process. The activation of another Cl- transport pathway on the apical membrane by prostaglandin E1 was suggested by Cl- uptake studies. Our findings indicate that the prostaglandin E1-stimulated Cl- secretion, which is associated with an increase in cyclic AMP level, intimately involves (a) a bumetanide-sensitive Na+,K+,Cl- cotransport pathway that serves as a Cl- uptake step across the basolateral membrane, (b) the stimulation of a barium-sensitive K+ efflux mechanism on the basolateral membrane that most likely acts to recycle K+, and (c) the activation of a Cl- transport pathway on the apical membrane that serves as a Cl- exit pathway.

Alprostadil↗
PubMed2005

Guanylin and E. coli heat-stable enterotoxin induce chloride secretion through direct interaction with basolateral compartment of rat and human colonic cells.

We previously detected specific binding activity of Escherichia coli heat-stable enterotoxin (ST), the guanylin exogenous ligand, in rat colonic basolateral membranes. Because guanylin circulates in the bloodstream, we tested the hypothesis that it modulates intestinal ion transport by acting on the serosal side of intestinal cells. The effects of the mucosal and serosal addition of ST and guanylin on ion transport were investigated in the rat proximal colon and in Caco-2 cells in Ussing chambers, by monitoring short-circuit current (Isc). cGMP concentration was measured in Caco-2 cells by RIA. Mucosal ST addition induced an increase in Isc in rat proximal colon consistent with anion secretion. Serosal addition induced the same effects but to a lesser extent. The electrical effects observed in Caco-2 cells paralleled those observed in rat proximal colon. A pattern similar to the electrical response was observed with cGMP concentration. Guanylin addition to either side of Caco-2 cells induced the same effects as ST, although to a lesser extent. In all conditions, the electrical effect disappeared in the absence of chloride. ST directly interacts with basolateral receptors in the large intestine inducing chloride secretion through an increase of cGMP. However, the serosal effects are less pronounced compared with those observed with mucosal addition. Guanylin shows the same pattern, suggesting that it plays a role in the regulation of ion transport in the colon, but the relative importance of serosally mediated secretion remains to be determined.

Animals↗
PubMed2002

Sodium-phosphate symport by Aplysia californica gut.

Phosphate transport across plasma membranes has been described in a wide variety of organisms and cell types including gastrointestinal epithelia. Phosphate transport across apical membranes of vertebrate gastrointestinal epithelia requires sodium; whereas, its transport across the basolateral membrane requires antiport processes involving primarily chloride or bicarbonate. To decipher the phosphate transport mechanism in the foregut apical membrane of the mollusc, Aplysia californica, in vitro short-circuited Aplysia californica gut was used. Bidirectional transepithelial fluxes of both sodium and phosphate were measured to see whether there was interaction between the fluxes. The net mucosal-to-serosal flux of Na+ was enhanced by the presence of phosphate and it was abolished by the presence of serosal ouabain. Similarly, the net mucosal-to-serosal flux of phosphate was dependent upon the presence of Na+ and was abolished by the presence of serosal ouabain. Theophylline, DIDS and bumetande, added to either side, had no effect on transepithelial difference or short-circuit current in the Aplysia gut bathed in a Na2HPO4 seawater medium. However, mucosal arsenate inhibited the net mucosal-to-serosal fluxes of both phosphate and Na+ and the arsenate-sensitive Na+ flux to that of phosphate was 2:1. These results suggest the presence of a Na-PO4 symporter in the mucosal membrane of the Aplysia californica foregut absorptive cell.

Animals↗
PubMed1979

Solute transport process in intestinal epithelial cells.

In rat small intestine, the active transport of organic solutes results in significant depolarization of the membrane potential measured in an epithelial cell with respect to a grounded mucosal solution and in an increase in the transepithelial potential difference. According to the analysis with an equivalent circuit model for the epithelium, the changes in emf's of mucosal and serosal membranes induced by active solute transport were calculated using the measured conductive parameters. The result indicates that the mucosal cell membrane depolarizes while the serosal cell membrane remarkably hyperpolarizes on the active solute transport. Corresponding results are derived from the calculations of emf's in a variety of intestines, using the data that have hitherto been reported. The hyperpolarization of serosal membrane induced by the active solute transport might be ascribed to activation of the serosal electrogenic sodium pump. In an attempt to determine the causative factors in mucosal membrane depolarization during active solute transport, cell water contents and ion concentrations were measured. The cell water content remarkably increased and, at the same time, intracellular monovalent ion concentrations significantly decreased with glucose transport. Net gain of glucose within the cell was estimated from the restraint of osmotic balance between intracellular and extracellular fluids. In contrast to the apparent decreases in intracellular Na+ and K+ concentrations, significant gains of Na+ and K+ occurred with glucose transport. The quantitative relationships among net gains of Na+, K+ and glucose during active glucose transport suggest that the coupling ratio between glucose and Na+ entry by the carrier mechanism on the mucosal membrane is approximately 1:1 and the coupling ratio between Na+-efflux and K+-influx of the serosal electrogenic sodium pump is approximately 4:3 in rat small intestine. In addition to the electrogenic ternary complex inflow across the mucosal cell membrane, the decreases in intracellular monovalent ion concentrations, the temporary formation of an osmotic pressure gradient across the cell membrane and the streaming potential induced by water inflow through negatively charged pores of the cell membrane in the course of an active solute transport in intestinal epithelial cells are apparently all possible causes of mucosal membrane depolarization.

Animals↗
PubMed2000

Comparison of different diagnostic methods for lupus pleuritis and pericarditis: a prospective three-year study.

BACKGROUND AND PURPOSE: Pleural or pericardial effusions, or both, are commonly encountered, but the differential diagnosis is sometimes difficult. We evaluated the diagnostic value of effusion immunofluorescent antinuclear antibody (ANA) titer, systemic lupus erythematosus (SLE) latex agglutination slide test, and cytologic LE cell examination in patients with pleural and/or pericardial effusions of various etiologies. METHODS: A total of 153 pleural and/or pericardial effusion specimens were collected by aspiration from 152 patients (14 SLE and 138 non-SLE patients). All specimens were sent for routine biochemistry testing, determination of ANA titer, SLE latex agglutination slide test, and LE cell examination. RESULTS: Ten of the 14 SLE patients had lupus serositis and all of them had high ANA titers (> or = 1:160) in their effusions. SLE latex and LE cell tests were positive in seven and eight patients with lupus serositis, respectively. The remaining four SLE patients with effusion of etiologies other than lupus serositis had low or negative effusion ANA titers. Among the non-SLE patients, 29 of 112 patients (26%) with pleural effusion and six of 26 patients (23%) with pericardial effusion had positive ANA tests (> or = 1:40). None of them had a positive SLE latex or LE cell test result. Thirteen of the 138 non-SLE patients (11%) had high effusion ANA titers (> or = 1:160). Effusion in 11 of 13 non-SLE patients (85%) was due to malignancy. CONCLUSIONS: Effusion ANA titer detection is a very sensitive but nonspecific test for the diagnosis of lupus serositis. SLE latex and cytologic LE cell tests can aid in the differential diagnosis as complementary tools. The specificity, positive and negative predictive values of these two tests are excellent for the diagnosis of lupus serositis.

Adolescent↗
PubMed1990

Effects of H+ and HCO3- secretion on mucus gel pH in isolated antral mucosa of bullfrog stomach.

To study the mechanism of self-protection of the gastric surface epithelium, we measured the pH gradient of the mucus gel layer in the isolated bullfrog antral mucosa with pH-sensitive microelectrodes in the Ussing chamber preparation. Under the control condition of 15mM HCO3- and 1.5% CO2 serosal perfusion, the pH on the interface between luminal solution and mucus gel layer (pHLMI) was 6.04 +/- 0.12 (n = 7), and the pH on the interface between the mucus gel layer and epithelial cell (pHMEI) was 5.69 +/- 0.13 (n = 7). When gastric acid secretion was stimulated by histamine (10(-4) M), the pHLMI became 5.43 +/- 0.12 (n = 4) and the pHMEI 4.40 +/- 0.18 (n = 4). Inhibition of acid secretion by cimetidine (10(-4) M) raised the pHLMI to 6.51 +/- 0.07 (n = 7) and the pHMEI to 6.23 +/- 0.08 (n = 7). Omeprazole (10(-4) M) also raised the pHLMI and the pHMEI to 6.78 +/- 0.13 (n = 7) and 6.56 +/- 0.13 (n = 7), respectively. These data suggested that the H+ ions secreted from the oxyntic cells were able to diffuse to the lateral side within the mucus gel layer, affecting the local pH just above the surface epithelial cells. Under high serosal HCO3- condition (45mM HCO3- and 1.5% CO2 in serosal side), the pHLMI and the pHMEI were elevated to 7.22 +/- 0.10 (n = 7) and 6.92 +/- 0.10 (n = 7), respectively. This result suggested that HCO3- secretion, which was served to neutralize the invading acid, depended upon the supply of HCO3- from the serosal medium. Thus, the serosal HCO3- would be working not only in the acid-protection, but also in the maintenance of pH gradient across the mucus gel layer.

Acid-Base Equilibrium↗
PubMed1989

Water flow in the toad urinary bladder in response to vasopressin: role of potassium.

In agreement with previous reports, we found that absence of K+ from the serosal bath of the toad urinary bladder substantially impairs vasopressin and cAMP-stimulated water flow. The decreased response to vasopressin appears unrelated to prostaglandin production since inhibition of endogenous prostaglandins by pretreatment with naproxen 10(-5) M failed to prevent the effect seen with K+-free Ringer's. The resistance to vasopressin does not appear to be directly related to epithelial K+ concentrations, in that maneuvers leading to decreased intracellular K+ failed to produce a similar effect. A more likely explanation appears to be that K+-free Ringer's induces an increased cytosolic Ca++ which, in turn, decreases the hydrosmotic effects of vasopressin. Several lines of evidence argue in favor of such an explanation: (a) Increased cytosolic Ca++ had been found in other tissues with low extracellular K+; (b) The resistance to vasopressin decreases with decreased serosal Ca++; (c) The effects of K+-free Ringer's are not additive in situations believed to have increased epithelial Ca++, i.e. replacement of serosal Na+ with choline; (d) The effects of K+-free serosal bathing medium could be both prevented and/or reversed if already established by increasing serosal bath, and presumably intracellular, pH, which is believed to decrease intracellular Ca++.

Animals↗
PubMed1981

[Intestinal absorption of vitamin B6 in vitro in response to the mucosal concentration of pyridoxine . HCl (author's transl)].

The in vitro absorption of vitamin B6 from the mucosal to the serosal solution was studied, using everted sacs of the proximal jejunum of male rats. The concentration and the absorbed amount of vitamin B6 in the intestinal wall and in the serosal solution was measured after an incubation of 45 minutes with 0, 2, 4, 10, 25, 50, 100, 200, 500 micrograms pyridoxine . HCl (PN . HCl) per ml mucosal solution. The concentration and the absorbed amount of vitamin B6, increased linearly with the mucosal concentration of PN . HCl. This could be found for the results of the serosal solution as well as for the results of the intestinal wall, which increased, however, more than those of the serosal solution. The passive diffusion was confirmed as mechanism of the absorption of vitamin B6. Besides, it could be concluded from these results that a homeostatic regulation of vitamin B6 is not due to the mucosal to serosal absorption.

Animals↗
PubMed1981

Electromyogram of rabbit colon and cecum in vitro.

The rabbit colon is unique in that the proximal colon has taenia coli, but the distal colon has none. Electromyograms were studied from the mucosal and serosal sides of the proximal (taenial) and distal (nontaenial) rabbit colon and cecum. In the proximal colon, similar electromyograms could be obtained from either the mucosal (circular muscle) or serosal (taenia coli) side. Spike bursts occurred in 18.6% of slow waves from the serosal side; however, there were none from the mucosal side. Unlike the proximal colon, the serosal side of the distal colon gave a better electromyographic recording which showed electrical silent periods and variable amplitudes of slow waves. Recordings could also be obtained equally well from both the mucosal and serosal sides of the rabbit cecum. Acetylcholine significantly increased (p less than 0.05) the percentage of slow waves with spikes in taenial colon and the electrical active period in nontaenial colon, whereas atropine, phenylephrine, isoproterenol, and tetrodotoxin produced a significant decrease (p less than 0.05). This study showed that the electromyograms of the rabbit colon and cecum were complex. Although differences existed between the taenial and nontaenial colon, they exhibited similar responses to some autonomic drugs. Furthermore, recordings could be obtained from both sides of the proximal colon and cecum.

Acetylcholine↗
PubMed1995

Host organ specifically determines cancer progression.

In order to further understand the role of the host organ in tumor progression, we have transplanted into nude mice histologically intact human colon cancer tissue on the serosal layers of the stomach (heterotopic site) and the serosal layers of the colon (orthotopic site). Xenograft lines Co-3, which is well differentiated, and poorly differentiated COL-3-JCK were used for transplantation. After orthotopic transplantation of the human colon tumors on the nude mouse colon, the growing colon tumor resulted in macroscopically extensive invasive local growth in 4 of 10 mice, serosal spreading in 9 of 10 mice, musclaris propria invasion in 1 of 10 mice, submucosal invasion in 3 of 10 mice, mucosal invasion in 3 of 10 mice, lymphatic duct invasion in 4 of 10 mice, regional lymph node metastasis in 4 of 10 mice, and liver metastasis in 1 of 10 mice. In striking contrast, after heterotopic transplantation of the human colon tumor on the nude mouse stomach, a large growing tumor resulted but with only limited invasive growth and without serosal spreading, lymphatic duct invasion, or regional lymph node metastasis. It has become clear from these studies that the orthotopic site, in particular the serosal and subserosal transplant surface, is critical to the growth, spread, and invasive and metastatic capability of the implanted colon tumor in nude mice. These studies suggest that the original host organ plays the same critical role in tumor progression.

Animals↗
PubMed1996

The secretory intestinal transport of some beta-lactam antibiotics and anionic compounds: a mechanism contributing to poor oral absorption.

The mechanisms of intestinal permeation of several beta-lactam antibiotics and anionic compounds were studied in vitro using excised rat intestinal segments. Permeation of cefazolin through jejunum, ileum and colon was highly secretory-oriented; serosal-to-mucosal permeation rates were two- to three-fold greater than mucosal-to-serosal permeation rates. Serosal-to-mucosal permeation decreased in the absence of D-glucose, and mucosal-to-serosal permeation increased, indicating that the preferential secretory transport of cefazolin is energy dependent. Ampicillin permeation across rat jejunum also favored secretion, whereas the permeation of cefaclor and cephradine favored absorption. Because cefazolin is anionic, several structurally unrelated anionic compounds were also tested. Of these only phenol red exhibited preferential serosal-to-mucosal permeation. The intestinal permeation of phenol red was concentration dependent and glucose dependent. Verapamil and a monoclonal antibody to P-glycoprotein only modestly and inconsistently affected the permeation of cefazolin, ampicillin and phenol red. Probenecid and guanidine were much more effective inhibitors of cefazolin and phenol red secretion. Mutual interactions between cefazolin and phenol red were also observed. These results show that the rat intestine has the capability for net secretory transport of some hydrophilic, anionic compounds. Transport of these compounds has some of the characteristics of organic anion and organic cation transport systems.

Ampicillin↗
PubMed1996

Development of a laboratory animal model of postoperative small intestinal adhesion formation in the rabbit.

In order to establish a model of postoperative intestinal adhesions that would simulate the problem experienced in horses, New Zealand White rabbits were utilized to compare two models of adhesion formation that had been successful in the horse, an ischemic strangulating obstruction (ISO) model and a serosal scarification model. An untreated control group was compared with animals subjected to 1, 2, 3 and 4 h periods of ISO, and to serosal scarification. At postmortem examination 14 d postoperatively, the number of rabbits in each group with adhesions was recorded. Serosal scarification was significantly more consistent at producing adhesions than ISO (Fisher's exact test, P = 0.0022). The 3 h of ISO group was significantly different from the control group: however, compared to the serosal scarification group, fewer animals had adhesions and one animal died of complications associated with the experimental procedure. Based on these results, serosal scarification was selected as the best model for utilization in further studies of adhesion prevention.

Animals↗
PubMed1997

Disruption of experimental fundic folds is prevented by interserosal scarring.

BACKGROUND: The main cause of recurrent reflux symptoms after Nissen fundoplication is disruption of the fundic wrap. Reoperation has shown a lack of scar tissue between the serosal surfaces of the fundic folds in these cases. METHODS: Attempts were made to induce serosal scarring during fundoplication performed in rabbits. In group 1 the serosal folds were attached to the upper fundus with three non-absorbable seromuscular sutures. In group 2 Teflon pledgets were placed between these sutures. Fibrin glue was injected between the folds in group 3 and polyglycolic acid mesh was inserted in group 4. RESULTS: When the rabbits were killed 6 months later, the serosa had unfolded and no macroscopic or microscopic scar tissue was found between the serosal surfaces, except in five of the six rabbits in group 3, in which fibronectin, laminin and collagen types I and III were present in interserosal scar tissue. CONCLUSION: Application of fibrin glue between the serosal surfaces of the fundic folds may prevent disruption of Nissen fundoplication.

Animals↗
PubMed1987

Non-invasive endoscopic technique to assess gastrointestinal perfusion.

Changes in mucosal blood flow may occur in many gastrointestinal disorders, but assessment is impossible without a non-invasive in vivo technique. We have compared endoscopic laser Doppler (LD) with oxygen electrode (OE) measurements in a dog isolated colon preparation, using variable perfusion measured with an electromagnetic flow probe. At maximum flow, LD measurements were made at three sites to compare mucosal with serosal readings. Flow rate was varied (1-38 ml/min) and measurements of microcirculatory flux obtained using LD, and of oxygen tension using a serosal OE. A progressive trend towards increasing flux was demonstrated from caecum to rectum-serosa: 46.8 +/- 18.7 V (caecum), 52.6 +/- 17.9 V (mid-colon) and 61.3 +/- 17.6 V (rectum). A parallel trend was observed in mucosal values: 41.1 +/- 18.2 V (caecum), 45.7 +/- 15.2 V (mid-colon) and 54.1 +/- 15.1 V (rectum). At all sites, serosal and mucosal values were not significantly different (Student's t test). LD serosal values correlated significantly with EM flow (r = 0.544, 0.01 greater than P greater than 0.001). A similar linear correlation was found between OE and EM flow (r = 0.65, P less than 0.001). Oxygen tension measurements varied as expected with microcirculatory flux (r = 0.441, 0.02 greater than P greater than 0.01). Endoscopic LD assessment of colonic microcirculation accurately reflects changes in blood flow.

Animals↗
PubMed1992

Effects of cytochalasin, colchicine, and ethylenediaminetetraacetic acid on linoleic acid transport across rat jejunal enterocytes.

The involvement and the site of interference of the cytoskeleton in the transport of linoleic acid across the rat jejunum was investigated by administration of microfilamentous and microtubular altering agents such as cytochalasin, colchicine, and ethylenediaminetetraacetic acid (EDTA). An isolated jejunal segment was perfused with a buffer containing labeled linoleic acid, and portal blood and perfusate samples were collected concomitantly at 5-min intervals and assayed for their radioactivity. At the end of the perfusion, the amount of radioactivity retained in the intestine was also determined. The results were analyzed by using a three-compartment physical model that allows the determination of mucosal and serosal permeability coefficients, from which changes in the permeability of the mucosal and serosal membranes were assessed. Cytochalasin decreased the permeability of the mucosal membrane to linoleic acid, but not that of the serosal membrane. The administration of colchicine, EDTA, or cytochalasin + colchicine increased the permeability of the serosal membrane but did not affect the mucosal membrane.

Animals↗
PubMed2002

Intestinal transport of the lactokinin Ala-Leu-Pro-Met-His-Ile-Arg through a Caco-2 Bbe monolayer.

ACE inhibitory peptides are biologically active peptides that play a role in blood pressure regulation. When derived from food proteins during food processing or gastrointestinal digestion, these peptides could function as efficient agents in treating and preventing hypertension. However, in order to exert an antihypertensive effect by inhibition of the ACE enzyme, they have to reach the bloodstream intact. The aim of this research was to assess if the known ACE inhibitory peptide Ala-Leu-Pro-Met-His-Ile-Arg, derived from a tryptic digest of beta-lactoglobulin, could be absorbed through a Caco-2 Bbe cell monolayer in an Ussing chamber and reach the serosal side undegraded. Samples of the mucosal compartment showed high ACE inhibitory activity. No or only little ACE inhibitory activity was detected in the serosal compartment. However, when the serosal sample was concentrated three-fold, a substantial ACE inhibitory activity was registered. Concomitantly, HPLC and MS clearly showed the presence of Ala-Leu-Pro-Met-His-Ile-Arg in the mucosal compartment, whereas in the serosal compartment only MS was able to detect the heptapeptide. In conclusion. under the observed experimental conditions, the ACE inhibitory peptide Ala-Leu-Pro-Met-His-Ile-Arg was transported intact through the Caco-2 Bbe monolayer, but in concentrations too low to exert an ACE inhibitory activity.

Amino Acids↗