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PubMed1983

The effect of barium chloride on intestinal secretion in the rat.

The addition of BaCl2 to the serosal solution, at concentrations from 0 X 25 mM to 10 mM, caused increases in potential difference, short-circuit current and resistance across stripped sheets of rat mid-intestine, although mucosal application had little effect. The response to BaCl2 was significantly greater than that obtained with the same concentration of CaCl2. An increase in net Cl- secretion entirely accounted for the rise in short-circuit current induced by BaCl2. BaCl2 inhibited net fluid uptake by everted sacs. It also enhanced the accumulation of fluid by intestinal loops in vivo and this was associated with an increased potential difference. The response to BaCl2 in vitro was not reduced in the absence of serosal Ca2+ ions. The effect of BaCl2 was abolished by trifluoperazine and also by TMB-8 (8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate hydrochloride). BaCl2 did not alter cyclic AMP production by isolated enterocytes. It is concluded that BaCl2 induces intestinal secretion by releasing Ca2+ from intracellular stores which then combines with calmodulin to stimulate the secretory process.

Animals↗
PubMed1994

The contribution of intestinal secretion to the dose-dependent absorption of celiprolol.

The contribution of the intestine to the nonlinear absorption of celiprolol in the rat was studied. After intravenous administration of 14C-celiprolol to bile duct-cannulated rats, approximately 9% of the dose was found to be associated with intestinal tissue and its contents. Microhistoautoradiography of frozen intestinal sections showed a time-dependent secretion of celiprolol from the blood into the lumen of the rat intestine. Propranolol, a lipophilic beta-blocker, was also found to be secreted into the intestine in vivo and transported in epithelial cells in both a temperature- and a pH-dependent manner, although to a lesser extent than celiprolol. Consistent with the observations in rats, transport of celiprolol from the basal-lateral to the apical side was found to dominate apical-to-basal transport using human Caco-2 cell monolayers. Additionally, using isolated rat small intestinal epithelial cells, celiprolol was found also to have a time- and temperature-dependent uptake, suggesting the involvement of a carrier-mediated system in its uptake. The uptake was inhibited by 2 mM celiprolol and propranolol and was also found to be pH dependent. Saturation of the carrier-mediated secretion of celiprolol in the intestine may result in enhanced absorption of celiprolol at high doses and account for its observed nonlinear absorption.

Animals↗
PubMed1990

CCK-releasing activity of rat intestinal secretion: effect of atropine and comparison with monitor peptide.

A bioassay for studying the cholecystokinin (CCK)-releasing activity of intraluminal protease-sensitive bioactive peptides was developed. In conscious rats, bile and pancreatic juice were chronically diverted from the proximal intestine to the ileum to cause chronic stimulation of CCK release and pancreatic protein secretion. CCK-releasing activity of test substances was assayed during transient inhibition of CCK release by intraduodenal sodium taurocholate (78 mumols/h). Intestinal secretion as a source of the putative trypsin-sensitive intestinal CCK-releasing peptide was obtained by rapid intestinal perfusion of isolated Thiry-Vella fistulae of jejunum in conscious rats, collected with or without atropine pretreatment. Partially purified rat pancreatic secretory trypsin inhibitor (PSTI, or "monitor peptide") was compared with ovomucoid trypsin inhibitor (OMTI) and with concentrated jejunal secretions for CCK-releasing activity and trypsin inhibitor activity. Concentrated, heat-treated jejunal secretions were the strongest stimulants of CCK release and pancreatic protein secretion in this model. OMTI had no CCK-releasing activity in this model, whereas a larger amount (approximately 5x, based on trypsin inhibitor activity) of PSTI weakly but significantly stimulated CCK release. CCK-releasing activity manifested by pancreatic protein secretion was equivalent in intestinal washes from atropine-treated and control Thiry-Vella fistula donor rats. Concentrated jejunal secretions had no trypsin inhibitory activity, indicating that the putative intestinal CCK-releasing peptide and "monitor peptide" are different substances.

Animals↗
PubMed2002

Intestinal secretion is a major route for parent ivermectin elimination in the rat.

The transepithelial intestinal elimination of ivermectin was studied using the intestinal closed-loop model in the rat. The common bile duct was cannulated, and duodenum, jejunum, and ileum were isolated in situ with their intact blood supplies. Following administration of 100, 200, or 400 microg/kg b.wt. ivermectin via the carotid artery, the elimination of parent ivermectin into the small intestinal lumen over 90 min was approximately 5-fold higher than in bile. The major amount of secreted ivermectin was recovered in the jejunum, but the duodenum showed a higher intestinal elimination capacity than the other intestinal segments with respect to the intestinal length. Systemic coadministration of the P-glycoprotein blocker verapamil significantly reduced the elimination capacity of jejunum by 50%, which resulted in a 30% decrease of ivermectin overall elimination by the small intestine. In contrast, verapamil did not significantly affect ivermectin secretion in duodenum, ileum, or bile in the same animals. Ivermectin small intestinal and biliary clearances were estimated to account for 27 and 5.5% of the total drug clearance, which was evaluated from a parallel in vivo experiment in which rats were given 200 microg/kg b.wt. ivermectin intra-arterially. In conclusion, intestinal secretion plays a greater role than biliary secretion in the overall elimination of ivermectin in the rat, providing major amounts of active drug to the intestinal lumen and to feces. This is discussed in terms of therapeutic efficacy against intestinal parasites in humans and animals and of ecotoxicity resulting from the contamination of livestock dung with parent drug.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1986

Involvement of the enteric nervous system in the intestinal secretion induced by sodium deoxycholate and sodium ricinoleate.

Rat small intestine was continuously perfused for up to 3 h with two different concentrations of sodium deoxycholate (4 and 8 mM) or with sodium ricinoleate (6 mM). The 4-mM bile salt solution produced a secretion that developed to a maximal rate within 3 h, whereas the maximal rate was reached within 1 h with the 8-mM bile salt solution. Hexamethonium, a ganglionic blocker, and lidocaine, a local anesthetic, always reduced the net fluid secretion to approximately zero irrespective of the rate of bile-salt-induced secretion, the concentration of the bile salt, or the perfusion time. Fluid secretion induced by sodium ricinoleate was, like the bile-salt-induced secretion, markedly inhibited by hexamethonium and lidocaine but not by atropine. It is concluded that the rate of secretion induced by the bile salt is related to the monomer concentration of free bile salt molecules in close proximity to or within the intestinal epithelium. The intestinal fluid secretion is mainly due to stimulation of an active secretory process via an activation of enteric nerves. Sodium ricinoleate evokes secretion via similar nervous reflex mechanisms.

Animals↗
PubMed1980

Inhibition of intestinal secretion without reduction of cyclic AMP levels.

Net water transport by the jejunum of anaesthetized rats was measured together with jejunal cyclic AMP content. Vasoactive intestinal peptide stimulated secretion and elevated the cyclic AMP level. Morphine (10 mg/kg s.c.) inhibited the stimulated secretion but failed to depress the cyclic AMP accumulation. It is suggested that cyclic AMP may not be the mediator of intestinal fluid secretion. Alternatively, morphine may block the secretory effect of cyclic AMP elevated by vasoactive intestinal peptide.

Animals↗
PubMed1978

Inhibition of VIP-stimulated intestinal secretion and cyclic AMP production by somatostatin in the rat.

The effect of somatostatin on colonic secretion induced by 10(-8) M vasoactive intestinal peptide (VIP), 10(-2) M theophylline, and 2 X 10(-3) M dibutyryl cyclic AMP was studied in muscle-stripped everted open rat colon sacs. The secretory response to VIP, measured as the decrease in net absorptive flow rate (microliters 30 min-1 mg-1 of dry weight), was maximal and equalled the responses to theophylline or dibutyryl cyclic AMP. Somatostatin (10(-5) M) blocked completely the secretory response to VIP but only partially the secretory response to theophylline or dibutyryl cyclic AMP. This difference in the extent of inhibition suggested that somatostatin exerted an inhibitory effect both before and after the point of generation of intracellular cyclic AMP. In order to test the hypothesis that one component of the action of somatostatin involved inhibition of the production of cyclic AMP, measurements of this nucleotide were made in isolated rat colon cells. Control levels of cyclic AMP measured by radioimmunoassay (12.6 +/- 1.6 pmoles per 10(6) cells) were not affected by 10(-5) M somatostatin. VIP (5 X 10(-8) M) increased cyclic AMP levels 2-fold (P less than 0.01) and this increase was blocked by somatostatin. The results indicated that somatostatin inhibits colonic secretion by exerting effects at two sites: one site lies at, and another beyond, the point of generation of intracellular cyclic AMP.

Adenylyl Cyclase Inhibitors↗
PubMed1989

Kinins as mediators of intestinal secretion.

Kinins are small peptides that have diverse biological actions. Concentrations of kinins in the nanomolar or subnanomolar range induce intestinal smooth muscle contraction and evoke mucosal electrolyte secretion. Hyperkininemia is associated with effects on gastrointestinal motility and intestinal mucosal inflammation. Bradykinin and kallidin are the predominant kinins with effects on the gastrointestinal tract of mammals. Bradykinin stimulates chloride ion secretion by the guinea pig and rabbit ileum, rabbit colon, rat colon and monolayers of human HCA-7 cells. Kinins directly or indirectly stimulate phospholipase A2 and phospholipase C. Cells in the lamina propria of the mucosa (e.g., fibroblasts, mast cells, leukocytes), by liberating cyclooxygenase and lipoxygenase metabolites of arachidonic acid, are involved in the kinin response; direct effects on epithelial cells cannot be ruled out, however. Antagonists now exist for kinin receptors. Based on studies with these antagonists in smooth muscle preparations, two subgroups of kinin receptor have been identified. The B2-type receptor appears to be responsible for both the contraction of ileal muscle and ileal secretion. Kinins are probably more important as pathophysiological rather than as physiological mediators. They may amplify the effect of inflammatory products that induce intestinal secretion. The precise involvement of kinins in clinical mucosal secretory states and diarrhea will require quantitative assessment of their levels during each phase of mucosal inflammation. Additional studies on the mechanism of action of kinins will be essential in designing therapy to mitigate the symptoms associated with mucosal inflammation.

Animals↗
PubMed2003

Getting control of intestinal secretion: thoughts for 2003.

There has been a search for more than 20 years for agents that will directly inhibit intestinal secretory mechanisms and thereby reduce stool volume in patients with high volume watery diarrhoea. Recent work has highlighted the importance of neurohumoral mechanisms in the pathogenesis of diarrhoea, notably the role of 5-hydroxytryptamine, substance P, vasoactive intestinal polypeptide and neural reflexes within the enteric nervous system. Cholera toxin and Escherichia coli enterotoxins are known to invoke these mechanisms in some diarrhoeal states. This new dimension of intestinal pathophysiology has suggested possible novel targets for anti-secretory therapy including, 5-hydroxytryptamine receptor antagonists, substance P antagonists, vasoactive intestinal polypeptide antagonists and the possibility for potentiating the pro-absorptive effects of endogenous enkephalins by use of enkephalinase inhibitors. There now seems to be a real possibility that anti-secretory therapy will become more widely available in the future.

Diarrhea↗
PubMed1996

The lysine-1 analog of guanylin induces intestinal secretion and natriuresis in the isolated perfused kidney.

Guanylin is an endogenous peptide synthesized by several mammalian species that mimics the effects of a thermostable enterotoxin of Escherichia coli (STa: NTFYCCELCCNPACAGCY) in the gut. We have cloned a lysine-1 derivative of rat guanylin (Lys-1-NTCEICAYAACTGC) and tested its effects on ileal tissue membranes in Ussing chambers and in the isolated perfused rat kidney. Rabbit ileal mucosa membranes were mounted into a Ussing chamber and the effects of Lys-1 guanylin (Lys-1 G) and STa enterotoxin peptide on chloride secretion were determined by changes in short-circuit current (Isc). Lys-1 G (10 to 100 nM) showed a dose-dependent effect on chloride secretion with a maximal response estimated to be 52 microA/cm2. Lys-1 G mimics the effect of STa peptide, but the enterotoxin elicited a greater maximal effect of 120 microA/cm2 (P < 0.01). Lys-1 G (2.5 micrograms/ml) promoted an increase in both urine flow (from 0.13 +/- 0.07 to 0.40 +/- 0.01 ml g-1 min-1, N = 4; P < 0.05) and glomerular filtration rate (from 0.68 +/- 0.02 to 0.85 +/- 0.00 ml g-1 min-1, N = 4; P < 0.01) in the isolated perfused kidney and a reduction of the fractional reabsorption of sodium (from 76.0 +/- 0.03 to 59.5 +/- 0.85%, N = 4; P < 0.01). These maximal effects were accompanied by intense natriuretic effect observed 30 and 60 min after drug administration. The Lys-1 G analog similar to STa enterotoxin elicited intestinal chloride secretion and a natriuretic effect. These data demonstrate that the cloned peptide analog retains the biological activity of the native hormone and presents activity similar to STa. The properties of Lys-1 G resemble those of a factor formed during perfusion of the hypoxic rabbit kidney and named by us factor natriureticus similis (FNS).

Animals↗