From transcription to cell surface expression, the induction of MHC class II I-A alpha by interferon-gamma in macrophages is regulated at different levels.

Using mouse bone marrow-derived macrophages we determined the role of interferon (IFN)-gamma at the different steps in expression of the I-A alpha chain of MHC class II molecules, from transcription to the cell surface. Levels of transcription, RNA, and protein were low in cells not stimulated with IFN-gamma. Treatment with IFN-gamma for 24 or 48 h induced an increase in mRNA levels (7- and 12-fold) that did not correlate with the increase in transcription (2.5- and 2.7-fold). The half-life of mRNA was not modified by IFN-gamma. These data suggest a block at the level of translation. In fact, IFN-gamma increased ribosome loading, which confirms regulation at the translational level. Treatment with IFN-gamma increased protein synthesis (6-fold after 48 h) and level of expression at the cell surface (3- and 9-fold after 24 and 48 h, respectively). Interestingly, treatment with IFN-gamma also increased the I-A alpha protein half-life from 2 to 6-7 h. This is the first attempt to determine qualitatively and quantitatively the regulation of an inducible gene at all the putative levels of control. The data indicate that IFN-gamma plays a critical role in MHC class II protein expression in macrophages through the regulation of different steps, from transcription to surface expression.

The expression of MHC class II genes in macrophages is cell cycle dependent.

Using different drugs, we stopped the cell cycle of bone marrow-derived macrophages at different points. After IFN-gamma stimulation, macrophages arrested at the G(1) phase of the cell cycle did not increase cell surface expression of the MHC class II IA. This inhibition is specific, because, under the same conditions, IFN-gamma induces the expression of Fcgamma receptors and the inducible NO synthase mRNA. Treatments that inhibit macrophage proliferation by blocking the cell cycle at the G(1) phase, such as adenosine, forskolin, or LPS, blocked the IFN-gamma induction of IA. Under IFN-gamma treatment, the steady-state levels of IAalpha and IAss mRNA did not increase in cells arrested at the G(1) phase and the half-life of the MHC mRNA was not modified. These data suggest that the cell cycle modulation of IFN-gamma-induced MHC II gene expression occurs at the transcriptional level. The expression of the class II transactivator mRNA induced by IFN-gamma was also blocked when macrophages were arrested at the G(1) phase of the cell cycle, suggesting that the lack of IFN-gamma response occurs at the early steps of MHC class II expression. Finally, macrophages arrested at the G(1) phase showed increased basal levels of cell surface IA due to an increase of the translational efficiency. These data show that the expression of MHC class II genes is regulated by the cell cycle.

LPS upregulates MHC class II I-A expression in B lymphocytes at transcriptional and at translational levels.

Major histocompatibility complex (MHC) class II molecules are expressed in a limited number of cell types, including B lymphocytes, dendritic cells and macrophages. Lipopolysaccharide (LPS) increases the surface expression of class II molecules in a murine B-cell line by inducing an increase in I-A protein and I-A mRNA levels. LPS does not modify the rate of mRNA degradation; therefore, the increase in mRNA is due to an increase in transcription. In addition, LPS increases the levels of I-Aalpha protein, which correlates with an increase in ribosome loading for I-Aalpha but not for I-Abeta mRNA after treatment with LPS. Interestingly, in non-induced cells, I-Aalpha messenger RNA shows a significant peak of free mRNA. Therefore, LPS regulates the expression of MHC class II molecules at translational level in B cells, in addition to the transcriptional control. The actual mechanism implies changes of translation initiation rates, as shown by an increase ribosome loading in polysome gradients.

Adrenergic and purinergic components in bisected vas deferens from spontaneously hypertensive rats.

1. Purinergic and adrenergic components of the contractile response to electrical field stimulation (EFS) have been investigated in epididymal and prostatic portions of Wystar Kyoto (WKY) and spontaneously hypertensive rat (SHR) vas deferens. 2. In both halves of SHR and WKY vas deferens, EFS (40 V, 0.5 ms for 30 s, 0.5-32 Hz) evoked frequency-related contractions. The neurogenic responses were biphasic, consisting of a rapid non-adrenergic response, dominant in the prostatic portion, followed by a slow tonic adrenergic component, dominant in the epididymal half. 3. Phasic and tonic components of the frequency-response curves evoked by EFS were significantly higher in the epididymal but not in the prostatic portion of vas deferens from SHR compared to WKY rats. 4. The alpha1-adrenoceptor antagonist prazosin (0.1 microM) was more effective against both components of the contractile response in the epididymal end of SHR than in WKY rats. 5. Inhibition by alpha, beta-methylene adenosine 5'-triphosphate (alpha,beta-meATP 3 and 30 microM) was higher in both components of the contractile responses in WKY preparations than in SHR. 6. Combined alpha1-adrenoceptor and P2x-purinoceptor antagonism virtually abolished the EFS-evoked contractile response in both strains. The degree of inhibition by prazosin (0.1 microM) after P2x-purinoceptor blockade was higher in SHR than in WKY rats. 7. These results demonstrate a modification in the purinergic and noradrenergic contribution to neurogenic responses in SHR and WKY animals besides a co-participation of ATP and noradrenaline in both contractile components of the response to EFS.

Translational control of MHC class II I-A molecules by IFN-gamma.

MHC class II molecules are expressed in a limited number of cell types, including B lymphocytes and macrophages (M phi). IFN-gamma increases the surface expression of class II molecules in a murine B cell line without inducing detectable changes in either I-A or I-A mRNA levels. In bone marrow-derived M phi, IFN-gamma causes an increase in class II expression at both the mRNA and surface levels. In addition to the increase in transcription rates described for M phi, IFN-gamma increases the rate of synthesis of IA alpha and IA beta proteins and the ribosome loading for both mRNA molecules in both cell types. Interestingly, there is a significant peak of free I-A mRNA in noninduced cells. Therefore, IFN-gamma regulates the expression of MHC class II molecules at the translational level in both B cells and M phi and, as already reported, at the transcriptional level only in M phi. The actual mechanism of regulation causes changes in the translation initiation rates in both cell types, as demonstrated by an increase in ribosome loading in polysome gradients.

Contribution of inhibitory neurotransmitters to the CCK induced relaxation of the circular muscle of avian ileum.

The sulphated form of cholecystokinin-octapeptide (CCK-OP) induces a concentration-dependent relaxation of the circular muscle of isolated chicken ileum which is unaffected by atropine or propranolol but abolished by tetrodotoxin (TTX). The aim of this study was to investigate whether purinergic (ATP), nitrergic (NO) and peptidergic (VIP) neurons are implicated in the response to CCK-OP. In preparations prerelaxed with ATP, CCK-OP caused a further relaxation (average 46%). In addition, suramin (a P2 purinoceptor antagonist) inhibited the response to both ATP and CCK-OP. L-N(G)-nitroarginine (L-NO-Arg) reduced the response to CCK-OP, an effect which was reversed by L-arginine (L-Arg). In the presence of trypsin, the response to CCK-OP was markedly decreased (to about 10% of the original response). Moreover, in preparations prerelaxed with chVIP, the response to CCK-OP consisted of a small additional relaxation (average 15,7%). The responses to chicken VIP (chVIP) or sodium nitroprusside (NaNP), a NO donor, are TTX resistant whereas that to ATP is blocked by TTX. L-NO-Arg significantly reduced the relaxation induced by ATP, but did not change that induced by chVIP. The response to ATP after exposure of the tissue to maximal chVIP concentration was significantly reduced (average 25%). Our results suggest that the effects of CCK-OP seem to be mediated through purinergic neurons, which in turn would stimulate the release of NO and a peptide (possibly chVIP). ChVIP and NO interact with receptors located on muscle cells causing the relaxation of the circular muscle coat of the ileum.

CCK is involved in both peripheral and central mechanisms controlling food intake in chickens.

The aim of this work was to study the involvement of cholecystokinin (CCK) in the control of food intake in chickens. The following aspects were studied: 1) the effects of intravenous and intracerebroventricular sulfated octapeptide of CCK (CCK-8s) on voluntary food intake; 2) the effects of two CCK-receptor antagonists. L-365,260 and L-364,718, on food intake; and 3) the ability of such drugs to block the effects of CCK-8s on food intake in the chicken. Intravenous and intracerebroventricular CCK-8s caused a decrease in food intake. Intraperitoneal L-365,260, a CCK-receptor antagonist with low affinity for the two CCK receptors described in the chicken, increases food intake. Intracerebroventricular L-364,718, a drug that has high affinity for the chicken central CCK-receptor type, increased food intake. The effect of intravenous CCK-8s on food intake was not blocked by L-364,718 or L-365,260, whereas that of intracerebroventricular CCK-8s was blocked by intracerebroventricular L-364,718. It is concluded that central endogenous CCK plays a role in the control of food intake, which is dependent on central CCK-receptor type; nevertheless, peripheral CCK also decreases food intake acting on the peripheral CCK-receptor type. The fact that intracerebroventricular L-364,718 is able to increase food intake is related to its high affinity for the central CCK-receptor type of this species. Finally, three different speculations that might explain the fact that intraperitoneal L-365,260 increases food intake are discussed.

Effect of different calcium channel blockers on inhibitory junction potentials and slow waves in porcine ileum.

The effect of several calcium channel blockers was evaluated: (i) on spontaneous electrical and mechanical activities and (ii) on the response to electrical field stimulation. The study was carried out on whole-thickness preparation of porcine ileum. Glass microelectrodes were used to record membrane potential from smooth muscle cells. Resting membrane potential was -60 +/- 2mV (n = 18) and preparations generated spontaneous slow waves. Electrical field stimulation (EFS) was applied using different parameters. The amplitude and duration of inhibitory junction potentials (IJPs) increased with EFS strength. IJPs were abolished by tetrodotoxin (1 microM). Nifedipine (1 microM) did not modify the amplitude or duration of IJPs. The frequency of slow waves was not modified, however a slight but significant (p < 0.001) reduction in slow wave duration was observed. Mechanical activity was abolished in presence of nifedipine within approximately 6 min. omega-agatoxin IVA (50 nM) or omega-conotoxin MVIIC (100 nM), respectively a P-type and a Q-type calcium channel blockers, did not modify slow wave and IJP characteristics. In contrast, in presence of omega-conotoxin GVIA (100 nM), a N-type calcium channel blocker, or omega-conotoxin MVIIC (1 microM), IJPs were completely abolished. These data suggest that, in porcine ileum, N-type but not P-,Q- or L-type calcium channels are involved in the release of the non-adrenergic non-cholinergic neurotransmitters mediating IJPs. L-type calcium channels underlie electrical mechanical coupling but are not involved in slow wave generation.

Central and NO mediated mechanisms are involved in the inhibitory effects of CCK on the chicken cecorectal area.

In chickens CCK-8s induces defecation and causes an inhibition of rectal electrical activity (EA) and an increase in cecal motility. In contrast, CCK-4 inhibits the motility of both rectum and ceca. The cecorectal responses to CCK-8s and CCK-4, given intravenously (i.v.), were studied in conscious chickens prepared with electrodes for electromyography; the influence of atropine, phentolamine plus propranolol, hexamethonium and L-NAME on such responses was determined. Atropine and phentolamine plus propranolol did not cause any change in the response to CCK-8s or CCK-4 in the cecorectal area. Hexamethonium only induced a significant decrease in the number of defecations (ND) induced by CCK-8s. L-NAME slightly modified the decrease in rectal EA due to CCK-8s. The effects of intracerebroventricular (i.c.v.) administration of CCK-8s and CCK-4 were also studied. CCK-8s and CCK-4, given i.c.v., caused, in conscious chickens, a slight decrease in cecal EA, in the 15 minutes following administration. This effect was similar to that seen after i.v. administration of CCK-4. In conclusion, our results suggest that the inhibitory action of CCK on chicken rectum is mediated, at least in part, through nitric oxide release. In addition, nicotinic receptors mediate the increase in the ND caused by CCK-8s. Ganglionic, muscarinic, adrenergic and nitrergic blockade were not able to modify the excitatory cecal response to CCK-8s, which may indicate that the receptor mediating this effect is located on the cecal smooth muscle. Finally, the inhibitory action of i.v. CCK-4 on chicken cecum seems to be centrally mediated, as suggested by the fact that i.c.v. administration of either CCK-8s or CCK-4 induce a similar effect.

L-364,718 and L-365,260, two CCK antagonists, have no affinity for central benzodiazepine binding sites in chickens.

It has recently been demonstrated that L-365,260, a CCK-B antagonist in mammals, causes an increase in food intake in chickens. In contrast, L-364, 718, a CCK-A antagonist in mammals, shows this effect only at very high dose levels. It has been shown that L-365,260 has very low affinity for chicken CCK receptors. Thus, the mechanism of action of L-365,260 remains unknown. As L-365,260 is a benzodiazepine derivative, one may hypothesize that it would be acting on benzodiazepine binding sites. The aims of this work were to establish the existence of benzodiazepine binding sites in the chicken brain, and to check the possibility that L-365,260 was acting on these receptors, determining the affinity of L-364,718 and L-365,260 for them. We have found specific binding for tritiated flunitrazepam (a benzodiazepine agonist) ([3H]-flunitrazepam) in chicken brain membranes. A single binding site was detected with a Kd of 3.58 +/- 0.97 nM and a Bmax of 451.6 +/- 23.3 fmol/mg protein L-365,260 and L-364,718 exhibited very low affinity for these binding sites (Ki = 1.17 x 10(-6) +/- 0.16 x 10(-6) M and Ki > 10(-5) M, respectively). Thus, these results demonstrate that the increase in food intake caused by L-365,260 in the chicken is not due to a direct action on benzodiazepine receptors. Other possible explanations for its effect are discussed.

Central and peripheral cholecystokinin receptors in chickens differ from those in mammals.

Specific binding for the radioligand [3H]CCK-8s has been identified in chicken brain, hypothalamus, pancreas, gallbladder and caecum membranes. This binding was found to be of high affinity, low capacity and saturable, suggesting the presence of specific CCK receptors in these tissues. Scatchard analysis indicated the existence of a single binding site for each tissue. Dissociation constant (kd) values were 0.63 +/- 0.18, 0.73 +/- 0.13, 0.85 +/- 0.12, 1.47 +/- 0.21 and 0.96 nM for brain, hypothalamus, pancreas, caecum and gallbladder, respectively. Binding densities (Bmax) were higher for brain, pancreas and caecum (32.60 +/- 10.70, 30.33 +/- 2.40 and 35.83 +/- 5.10 fmol/mg protein, respectively) than for the other two tissues (9.75 +/- 1.90 and 6.31 fmol/mg protein for hypothalamus and gallbladder, respectively). As in mammals, CCK-4 shows high affinity for CCK receptors located in chicken brain and hypothalamus, and very low affinity for those located in peripheral structures. L-364,718 (a CCK-A antagonist) showed a relative selectivity and a high affinity for those receptors located in central tissues, whereas L-365,260 (a CCK-B antagonist) is almost inactive in all studied tissues. These results give support for the existence of at least two distinct CCK receptors in birds and that these receptors are relatively different from those described in mammals.

Intraluminal lipids modulate avian gastrointestinal motility.

Infusion of lipids into the ileum delays gastric emptying and intestinal transit time in some species. The aim of this study was to characterize the actions of intraluminal lipid infusion on gastrointestinal electrical activity in chickens. Animals were prepared for electromyography with chronic electrodes in stomach, duodenum, and small intestine. Two catheters were chronically placed in the esophagus and ileum to infuse equimolar doses of either oleic acid (OA) or triolein (TO). Both OA and TO, esophageally infused, inhibited the frequency of the gastroduodenal cycle and increased the frequency of antiperistaltic spike bursts in the duodenum. Ileal infusion of OA, but not of TO, produced the same effects. Both esophageal and ileal OA infusion increased the duration of the migrating myoelectric complex (MMC) and decreased the speed of propagation of phase III. In conclusion, intraluminal infusion of lipids modulates gastrointestinal motility by decreasing the frequency of the gastric cycle, increasing duodenogastric refluxes, and elongating the MMC. These actions could delay gastric emptying and increase transit time, which suggests the presence of an "ileal brake" mechanism similar to that described in mammals.

Modulation of the migrating myoelectric complexes by cholecystokinin and gastrin in the gastrointestinal tract of chickens.

Several mammalian avian species, including the chicken, show migrating myoelectric complexes (MMC) both in unfed and fed states. In these species, postprandial hormones seem to modulate but not to disrupt the MMC. To gain more information in this modulatory role, we evaluated the role of cholecystokinin (CCK) vs gastrin on the regulation of intestinal motility in chickens. Birds were implanted with eight electrodes for electromyography in the stomach, duodenum, jejunum, and ileum. In feed-deprived animals, CCK infusion (10(-12) mol/kg per min x 3 h) did not disrupt the MMC but induced changes in the MMC pattern similar to those induced by a meal. Infusion of CCK in fed animals induced dose-dependent effects: CCK infused at 10(-11) and 3 x 10(-11) mol/kg per min x 2 h, progressively elongated the MMC and slowed the speed of propagation of Phase 3. Furthermore, CCK infused at 10(-10) mol/kg per min x 2 h disrupted the MMC but a Phase 3 appeared just after the end of the infusion. By contrast, chicken gastrin (10(-10) mol/kg per min x 2 h) did not modify the MMC pattern. In conclusion, CCK influence on the intestinal motility of chickens ranges from the modulation of the MMC to total disruption, depending on the dose. Moreover, this study suggests that the mechanism of action of CCK could be similar in both mammalian and avian small intestines.

Is nitric oxide the final mediator regulating the migrating myoelectric complex cycle?

The main objective was to study the role of nitric oxide (NO) in the conversion of migrating myoelectric complexes (MMC) to the irregular electrical activity characteristic of the postprandial state. Both rats and chickens were implanted with electrodes for electromyography in the small intestine. Intravenous infusion of NG-nitro-L-arginine (L-NNA), a NO synthase inhibitor, induced an organized MMC-like pattern in fed rats. Infusion of sodium nitroprusside, a NO donor, disrupted the MMC, inducing a postprandial-like motor pattern in fasting rats. Similarly, in chickens L-NNA mimicked the fasting pattern, consisting of a shortening of phase II, enlargement of phase III, orad displacement of the origin of the MMC, and an increase in the speed of phase III propagation. An inhibition of NO synthesis seems to be involved in the induction of the fasting motor pattern, whereas an increase of NO mediates the occurrence of the fed pattern. It is suggested that NO might be the final mediator in the control of small intestine motor patterns.

Effects of cholecystokinin on chicken cecal motility: mechanisms involved.

The aims of this work are to characterize the effects of cholecystokinin (CCK) on chicken ceca and to study in vitro the mechanisms through which such actions are mediated. Longitudinal and circular cecal strips kept in vitro in organ baths were responsive to CCK sulphated octapeptide (CCK-8s). On longitudinal strips the response consisted of a fast phasic contraction followed by a sustained increase in tone which was dose dependent and decreased markedly in the presence of tetrodotoxin (TTX). Ketanserin (10(-5) M) also caused a decrease in the CCK-8s response. CCK tetrapeptide (CCK-4) and CCK unsulphated octapeptide (CCK-8ns) induced slightly less contractile effects at concentrations of 2 x 10(-6) M only. L365,260 and L364,718 decreased the response of longitudinal strips to CCK-8s with similar efficacy. On circular strips CCK-8s caused rhythmic phasic contractions of dose dependent amplitude and frequency, and both effects were resistant to TTX. The EC50 for the amplitude was about 4 times higher than that for the frequency. CCK-8ns (2x 10(-6) M) also caused phasic contractions, whereas the same concentrations of CCK-4 did not elicit any motor effects. L365,260 and L364,718 showed different efficacy in decreasing amplitude or frequency of contraction. These results suggest that 1) Both muscularly and neurally located CCK receptors are present on the longitudinal layer of chicken ceca whereas only muscular receptors are present on the circular muscle. 2) 5HT2 receptors seem to be involved in the neurally mediated CCK-8s response observed in the longitudinal layer. 3) The different potency of CCK-8s, CCK-8ns and CCK4 to induce contractile effects and of the CCK-A and CCK-B antagonists to block such effects suggests the existence of two different CCK receptors on the circular layer.

Experimental conditions affecting in vitro intestinal incorporation of palmitic acid: a methodological approach.

In the rat, a large number of in vitro studies on intestinal fatty acid uptake have been carried out. However, the results obtained under different experimental conditions are often contradictory. The present work is a critical approach to the experimental aspects which may modify in vitro intestinal uptake of fatty acids. Different kinds of intestinal tissue samples (intact, everted or opened rings) were used. The histological changes and the uptake of palmitic acid were measured for each type of sample under different stirring rates, at different incubation times and with micellar solutions of varying composition. It is concluded that 1) opened rings have the highest absorptive capacity with the lowest dispersion; 2) incubation periods longer than 30 minutes do not result in additional palmitic acid uptake and may lead to severe tissue hypoxia as indicated by extensive vacuolization; 3) stirring rates over 1 cycle/sec do not result in increased PA uptake and cause extensive mucosal disruption, particularly in jejunal samples.

Effects of temperature on in vitro palmitic acid uptake by chicken and rat intestinal tissue.

The intestinal absorption of fatty acids proceeds by simple or facilitated diffusion, a mechanism which is affected by temperature. However, most studies in this field have not taken into consideration the fact that birds have higher physiological temperature than mammals, the absorption being studied at 37 degrees C in both cases. The aim of this work has been to find out whether the higher palmitic acid (PA) uptake rate in birds (chickens) compared to mammals (rats) is attributable to the differences between their body temperatures (41.5 degrees C for chickens and 37.5 degrees C for rats). PA-uptake was studied in intestinal (ileal and jejunal) tissue samples of both Hybro broiler chickens (male and female, 4 weeks-old) and Ico:OFA rats (males and females, 8 weeks-old). The intestinal tissue samples were incubated in micellar solution (0.6 mM 14C-PA; 0.3 mM monoolein; 3.4 mM sodium taurodeoxycholate) at 37.5 degrees C and 41.5 degrees C in both cases. Chicken intestinal tissue incorporated PA with higher efficiency at 41.5 degrees C than at 37.5 degrees C. In contrast, increasing the incubation temperature to 41.5 degrees C led to a decrease in PA uptake by female rat intestinal tissue whereas specimens from male rats exhibited the same absorptive efficiency. These results suggest that the incubation temperature determines to some extent the efficiency of fatty acid uptake. However the fact that the temperature caused opposite effects in rats and chickens indicates that the changes in temperature affect the intracellular processing of the fatty acids already taken up rather than the diffusion of fatty acids through the enterocyte brush-border membrane.

Effects of oleic and elaidic acids on in vitro intestinal uptake of cholesterol in the rat.

The effects of oleic and elaidic acid upon the in vitro intestinal uptake of cholesterol were studied in 9 weeks-old male and female rats. Elaidic acid increases the uptake of cholesterol when compared to oleic acid in both males and females. It is suggested that elaidic acid may enhance the esterification of cholesterol within the enterocyte through being more available for esterification and/or through being preferentially incorporated into cholesterol esters.

Mechanisms mediating the effects of cholecystokinin on avian small intestine longitudinal smooth muscle.

The aims of this study were (1) to define the effects of CCK-8s and related peptides on chicken ileum longitudinal smooth muscle and (2) to explore the mechanisms by which such effects occur. The effects of CCK-8s were assayed in vitro on chicken longitudinal ileal strips. CCK-8s produced contraction of ileal strips (EC50 8.8.10(-9) M). CCK-8ns and CCK-4 did not have remarkable contractile effects even when added at concentrations 200-times higher than the EC50 for CCK-8s. L365,260 slightly inhibited the effects of CCK-8s whereas L364,718 was ineffective. Tetrodotoxin (10(-6) M) markedly decreased the effects of CCK-8s. Atropine (10(-6) M) did not modify the neurally mediated effects of CCK-8s, whereas ketanserin (10(-5) M) decreased the response to CCK-8s. Substance P-desensitized preparations exhibited reduced responses to CCK-8s. Our results indicate that CCK receptors present in chicken ileum behave similarly but not identically to the CCK-A receptor described in mammals. Most of these CCK receptors are neurally located but a minor proportion is also present on smooth muscle. The neurally mediated response to CCK-8s does not involve cholinergic mechanisms, but serotonin and substance P releasing neurons.

Rhythmic oscillating complex: characterization, induction, and relationship to MMC in chickens.

Migrating myoelectrical complexes (MMCs) and rhythmic oscillating complexes (ROCs) have been investigated in chickens prepared for electromyography. Animals were chronically implanted with electrodes in stomach, duodenum, jejunum, ileum, ceca, and rectum. MMCs showing phases I-III were found in the jejunum and ileum both in fed and fasted states. Repetitive spike bursts were recorded in the duodenum (0.5-1/h), disrupting the gastroduodenal coordination and preceding a phase III in the jejunum. ROCs appeared spontaneously in fasted animals and in 75% of the recordings during the dark period. Four consecutive intestinal myoelectrical patterns have been described during a ROC. Briefly, they consisted in series of high-speed propagated abroad contractions of great amplitude that progressively changed into others of orad direction. In relation to the MMC, the ROC pattern appeared just after a phase III reached the distal ileum, and a pattern of duodenal repetitive spike bursts, followed by a migrating phase III in the jejunum, started at the duodenum after a ROC. No myoelectrical changes were recorded in cecorectal activity during ROC. Vagotomized animals showed the ROC pattern. Neither apomorphine (5-100 micrograms/kg iv) nor cholecystokinin (10(-9) mol/kg iv) induced ROCs. Naloxone (5 x 10(-7) mol/kg iv) and atropine (0.1 mg/kg iv) induced isolated orad contractions. Myoelectrical and functional similarities can be found between retrograde giant contractions, described in mammals, and ROCs. However, they differ in their origin and mechanism of induction.