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R Serio

Publications and source records attributed to R Serio.

At least 19 recordsLinked to original sources
PubMed1992

Neurotensin: dual effect on the motor activity of rat duodenum.

The effects of neurotensin on mechanical activity of rat duodenum were investigated using an isometric-isovolumic preparation. Neurotensin (1 pM to 10 nM) induced a concentration-dependent, tetrodotoxin (TTX)-insensitive fall in both endoluminal pressure and isometric tension. At higher concentrations of neurotensin (1 nM to 1 microM) the relaxation was followed by a concentration-dependent TTX-insensitive contraction, detected only by an increase in endoluminal pressure. Different concentrations of neurotensin were required to desensitize the relaxant and the contractile actions of the neuropeptide. The relaxation was antagonized by apamin, while the contractile response was blocked by nifedipine. Neurotensin, when tested separately on longitudinal and circular muscular strips, caused relaxation of the longitudinal strips. Circular strips showed contractions in response to neurotensin, following an inhibitory phase, if the strips were spontaneously or pharmacologically activated. The results suggest the presence of two sets of neurotensin receptors with a differential localization between the two muscular layers in rat duodenum.

Animals↗
PubMed1992

On the peptidergic hypothesis for non-adrenergic non-cholinergic innervation in the rat duodenum.

1. The nature of the non-adrenergic, non-cholinergic (NANC) transmitter was studied in vitro in the rat duodenum, by use of an isometric-isovolumic preparation. 2. Electrical field stimulation (EFS) induced a tetrodotoxin (TTX)-sensitive fall both in luminal pressure and in isometric tension. 3. Neurotensin (NT) induced TTX-insensitive inhibitory responses similar to those induced by EFS. Vasoactive intestinal peptide (VIP) caused a delayed, slow, concentration-dependent, TTX-insensitive inhibitory effect, detected only by a change in luminal pressure. 4. alpha-chymotrypsin prevented the NT- and VIP-induced inhibitory effects and antagonized the response to EFS. 5. Apamin antagonized the EFS- and NT-induced effects, but failed to affect the relaxation in response to exogenous VIP. 6. Desensitization of NT receptors by exposure to NT (10 nM) for 30 min did not affect the EFS-induced relaxation. 7. These findings provide support for the involvement of a peptide in the NANC relaxation in rat duodenum. However, there is no evidence that NT or VIP are neurotransmitters released from the NANC system in this preparation.

Animals↗
PubMed1992

Non-adrenergic, non-cholinergic inhibitory responses to nerve stimulation in rat colonic circular muscle.

The nerve-mediated response to electrical field stimulation (EFS) in rat colonic circular muscle was investigated using the single sucrose-gap technique. EFS with a single pulse (0.4 ms, supramaximal voltage) elicited transient TTX-sensitive hyperpolarization (IJP) often followed by an 'off' depolarization associated with muscular contraction. No relaxation associated with the IJP could be seen unless tone was pharmacologically induced by carbachol (10(-6) M). IJPs were due to non-adrenergic, non-cholinergic (NANC) nerve activation since they were not affected by atropine (10(-7) M) or guanethidine (10(-6) M) superfusion. The mechanism underlying the IJP was presumably an increase in K+ conductance, and the NANC neurotransmitter might open largely apamin-sensitive, Ca(2+)-dependent K+ channels. Purines or vasoactive intestinal polypeptide (VIP) did not mimic the effects of NANC nerve stimulation. Therefore, the NANC inhibitory system, producing IJPs, in rat colonic circular muscle is not purinergic or VIPergic in nature.

Animals↗
PubMed1992

K(+)-channel blockers do not decrease acetylcholine depolarizations in canine trachealis.

Using the double sucrose gap, we have examined the role of K+ channels in the cholinergic depolarizations in response to field stimulation and acetylcholine (Ach) in canine trachealis. Acetylcholine-like depolarization per se decreased electrotonic potentials from hyperpolarizing currents. The net effect of acetylcholine (10(-6) M) depolarization on membrane conductance was a small increase after the depolarization was compensated by current clamp. Reversal potentials for acetylcholine depolarization and for the excitatory junction potential (EJP) were determined by extrapolation to be 20-30 mV positive to the resting potential, previously shown to be approximately -55 mV. They were shifted positively by tetraethylammonium ion (TEA) at 20 mM or Ba2+ at 1 mM. TEA or Ba2+ initially depolarized the membrane and increased membrane resistance. Repolarization of the membrane restored any reductions in EJP amplitudes associated with depolarization. After 15 min, the membrane potential partially repolarized, and acetylcholine-induced depolarization and contractions were then increased by TEA. 4-Aminopyridine depolarized the membrane but decreased membrane resistance. Apamin (10(-6) M), charybdotoxin (10(-7) M), and glybenclamide (10(-5) M) each failed to significantly depolarize membranes, increase membrane resistance, or reduce EJP amplitudes or depolarization to 10(-6) M Ach. Glybenclamide reduced depolarizations to added acetylcholine slightly. TEA occasionally reduced the EJP markedly, but this was shown to be most likely a prejunctional effect mediated by norepinephrine release. TEA alone among K(+)-channel blockers slowed the onset and the time courses of the EJP as well as the acetylcholine-induced depolarization. K(+)-channel closure cannot be a complete explanation of acetylcholine-induced membrane effects on this tissue. Acetylcholine must have increased the conductance of an ion with a reversal potential positive to the resting potential in addition to any effect to close K+ channels.

Acetylcholine↗
PubMed1991

Role of depolarization and calcium in contractions of canine trachealis from endogenous or exogenous acetylcholine.

The relationships of the electrical to the mechanical responses of the canine trachealis muscle during stimulation of its cholinergic nerves or exposure to exogenous acetylcholine were recorded in the single or the double sucrose gap. At 27 degrees C, the responses to a train of stimuli consisted of a transient depolarization excitatory junction potential of 10-30 mV followed by fading oscillations and contractions. When stimulus parameters were varied in the single sucrose gap, contractions were more closely associated with the occurrence of and varied in duration with the oscillations rather than with the amplitude of the EJP. Acetylcholine superfused at a concentration of 10(-6) M for 30 s caused a prolonged depolarization of 10-20 mV, but a much larger contraction than could be elicited by nerve stimulation. None of the responses to acetylcholine was significantly affected by the Ca channel antagonists, nifedipine, nitrendipine, or verapamil in Ca channel blocking concentrations. When tissues were exposed to a Ca-free medium, the excitatory junction potentials and oscillations rapidly disappeared, but the electrical and mechanical responses to acetylcholine persisted and only gradually disappeared with repetitive exposures. Furthermore, in a medium with normal Ca2+ in the double sucrose gap, depolarization by 10-15 mV with an applied current caused no contraction, and repolarization to the normal membrane potential during acetylcholine-induced contraction caused no relaxation. Tetraethylammonium ion (20 mM) depolarized the membrane, increased membrane resistance, and enhanced the secondary oscillations and contractions after field stimulation. No other K(+)-channel blocker tested (Ba2+, apamin, 4-aminopyridine, glibenclamide, charybdotoxin) had the effect of prolonging secondary oscillations.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Slow-wave activity in colon: role of network of submucosal interstitial cells of Cajal.

The present study compares the electrophysiological properties of two preparations dissected from the canine colon circular muscle layer: first, containing the submucosal network of interstitial cells of Cajal (ICC) with two to four associated smooth muscle cell layers, and second, a circular muscle preparation devoid of the submucosal ICC network. In the ICC-rich preparations, consistent slow-wave activity was observed with prolonged plateau potentials of approximately 10-s duration. The plateau potentials were sensitive to D 600. In approximately 45% of circular muscle preparations devoid of the submucosal ICC network (confirmed using electron microscopy) slow waves, of different waveshape, were recorded at frequencies identical to those in whole circular muscle preparations. These slow waves did not show a plateau potential. Compared with ICC-rich preparations with a resting membrane potential of about -80 mV, circular muscle preparations had lower membrane potentials, about -70 mV when active, and about -60 mV when quiescent. Heptanol (1 mM) electrically uncoupled cells, since it abolished electrotonic current spread and allowed measurement of the input resistance by intracellular current injection. Heptanol also affected ionic conductances. Heptanol abolished slow waves; the underlying mechanism needs further investigation. In the presence of heptanol, cells in the isolated ICC network and in circular smooth muscle preparations showed spontaneous hyperpolarizing potential fluctuations at a frequency of four to six per second. These oscillations were abolished by current-induced hyperpolarization and TEA (30 mM) and are therefore likely due to spontaneously active K+ conductance.

Alcohols↗
PubMed1991

[The structural organization of the human myocardium: the interrelation between myocardial fibers and interstitial connective tissue].

The complex tridimensional structure of the human ventricular myocardium has rarely been studied in the past. In the normal heart, in the lapse of time of few weeks of the embryonic life, a radical transformation from a chaotic plexiform organization to a complex tridimensional structure occurs. From then on, the ulterior growth of the myocardial fibres will only be dimensional and quantitative, because the spatial geometry is to be considered definitive. The role of the interstitial connective tissue in following the development of the myocardium, possibly inducing or influencing it, is still unclear. We have performed an histologic study on serial sections of the ventricular mass of 7 human embryos and fetuses, from 5 to 20 weeks of gestational age. The sections have been evaluated for their morphologic characteristics as evidentiated by histochemical (PAS, trichrome, Gomori silver technique) and immunohistochemical (myosin, actin, desmin, myoglobin, vimentin, fibronectin, smooth muscle cell, endothelial factor VIII) stainings. The results show that myocardial growth is mantellar, proceeding from the epicardium toward the endocardium, with progressive structural organization in strata, variably related one to the other depending upon the considered site of the ventricular mass. The interstitium grows in parallel to the myocardial growth, beginning with a thin network surrounding each fibre that progressively in time is transformed in a complexly arranged and more densely packed structure. The collagen fibres appear initially at epicardial level, particularly around the coronary vessels.(ABSTRACT TRUNCATED AT 250 WORDS)

Connective Tissue↗
PubMed1990

Evidence against purines being neurotransmitters of non-adrenergic, non-cholinergic nerves in rat duodenum.

The possible involvement of purines in the non-adrenergic non-cholinergic (NANC) relaxation of rat duodenum was studied using an isometric-isovolumic preparation. Purines (adenosine, AMP, ADP, ATP) induced a concentration-dependent, tetrodotoxin (TTX)-insensitive, fall in both endoluminal pressure and isometric tension. The relaxation induced by adenosine and by 2-chloroadenosine was selectively antagonized by 8-phenyltheophylline (1, 10 nM, 0.5 microM) and the ATP-induced relaxation was opposed by alpha, beta-methylene ATP (10 microM) and by reactive blue 2 (10 microM). Electrical field stimulation (EFS) caused TTX-sensitive inhibitory effects similar to those induced by ATP. None of the purinergic antagonists used were capable of affecting the EFS-induced relaxation. Our results indicate that both P1 and P2 purinoreceptors are present in muscle of the rat duodenum and are not involved in the NANC relaxation.

Adenosine↗
PubMed1990

Evidence that adenosine is not involved in the non-adrenergic non-cholinergic relaxation in the rat duodenum.

In rat isolated duodenal segments, adenosine induced, in the presence of atropine and guanethidine, a dose-dependent, long-lasting (about 20 s), tetrodotoxin (TTX)-resistant relaxation both in endoluminal pressure and in isometric tension. Electrical field stimulation (EFS) induced, in the presence of atropine and guanethidine, a TTX-sensitive short-lasting (about 6 s) relaxation followed by a sustained rebound contraction. Theophylline, a P1 receptor antagonist, at the concentration of 100 microM caused a marked inhibition of the adenosine-induced relaxation, while the EFS-induced relaxation was not modified. Our results suggest that adenosine induces relaxation of the rat duodenal smooth muscle acting on P1 receptors localized at muscular level. However, differences in the morphology and in the sensitivity to theophylline between adenosine- and EFS-induced relaxation ruled out adenosine as neurotransmitter of the non-adrenergic, non-cholinergic inhibitory system.

Adenosine↗
PubMed1990

On the purinergic system in rat duodenum: existence of P1 and P2 receptors on the smooth muscle.

In rat duodenum, in vitro, in the presence of atropine and guanethidine, ATP administration caused a tetrodotoxin-insensitive relaxation followed by a rebound contraction. A similar response was obtained also after electrical field stimulation (EFS) of non-adrenergic, non-cholinergic (NANC) nerves. alpha, beta-methylene-TP and theophylline antagonized the response to ATP, but they failed to affect the noradrenaline- and EFS-induced relaxation. These results suggest that P1 and P2 receptors are present in rat duodenum, but their activation is not responsible for the inhibitor effects due to the NANC nerves.

Adenosine Triphosphate↗
PubMed1988

Thromboxane effects on canine trachealis neuromuscular function.

The objective of this study is to determine which inflammatory mediators had direct effects on canine trachealis muscle neuromuscular control to identify candidate mediators of the hyperresponsiveness observed in vitro after O3 exposure. Studies were carried out in the sucrose gap at 29 degrees C and in the muscle bath at 37 degrees C. Leukotriene (LT) B4, LTD4, and prostaglandin (PG) D2 had neither direct nor significant effects on the excitatory junction potentials (EJP's), the secondary membrane potential oscillations, or the associated contractions that followed field stimulation of cholinergic nerves. U 46619, a stable analogue of thromboxane (Tx) A2, enhanced (10(-10)-10(-7) M) the duration and the amplitude of secondary oscillations and associated contractions without affecting the EJP's. In the muscle bath, U 46619 enhanced field-stimulated contractions; this was antagonized competitively by SQ 29548. In both the sucrose gap and the muscle bath, higher concentrations (10(-9) M and higher) caused direct effects, small depolarizations, and contractions. These effects of U 46619 were unaffected by indomethacin or guanethidine but were abolished by SQ 29548, an antagonist selective at TxA2-PGH2 receptors. U 46619 at 10(-9) M did not affect electrical or mechanical responses to acetylcholine and at 10(-9) M did not increase the sensitivity to acetylcholine. Platelet-activating factor (PAF) was inactive in all muscle-bath and most sucrose-gap experiments. In 7 of 20 of the latter, it caused effects qualitatively like those of U 46619, but whether it acted through release of TxA2 could not be tested because of the rapid tachyphylaxis to PAF. We conclude that TxA2 may mediate the hyperresponsiveness found in vitro after O3 treatment.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1987

Inhibitory influences of vagal afferences on the oesophageal EMG peristaltic pattern.

The influence of vagal afferents on the EMG peristaltic pattern was studied in pigeon oesophagus. Bilateral vagotomy did not abolish the primary peristalsis, but induced significant modifications of the peristaltic pattern parameters. Vagal afferent stimulation induced an inhibitory effect consisting of a temporary break or definitive block of the EMG peristaltic activity already in progress. Vagal afferent stimulation also induced a reduction of the spontaneous EMG activity and this effect was abolished either by glossopharyngeal bilateral section or ganglionic block. Likewise vagal afferent stimulation, the crop distension caused inhibitory effects on EMG peristaltic pattern. This effect was abolished by bilateral vagotomy. These results indicate that vagal afferents, originating from the crop, could influence the central neurons responsible for the peristaltic motor programme.

Afferent Pathways↗
PubMed1987

Pigeon oesophageal EMG activity: analysis of intramural neural control.

The effects of agonist and antagonist cholinergic and adrenergic drugs on spontaneous electrical activity of transverse muscular strips of pigeon cervical oesophagus were examined. Tetrodotoxin failed to affect EMG activity. Cholinomimetics produced excitatory effects. The response to carbachol was enhanced by hexamethonium and reversed into an inhibitory effect by atropine. Noradrenaline evoked a concentration-dependent, biphasic effect (inhibition at low and excitation at high concentrations). Isoproterenol induced inhibitory response unaffected by tetrodotoxin. Phenylephrine induced excitatory response completely antagonized by tetrodotoxin and partially opposed by atropine. It is concluded that: i) the oesophageal spontaneous EMG activity is myogenic; ii) the intramural neurons have no tonic influence on the spontaneous EMG activity; iii) in the intramural plexuses there are cholinergic excitatory-, non-cholinergic excitatory- and inhibitory neurons, with unknown neurotransmitter; iv) excitatory alpha-adrenoceptors, located on the nervous elements and inhibitory beta-adrenoceptors, located on the smooth-muscle cells, are present.

Action Potentials↗
PubMed1987

5-Hydroxytryptamine involvement in the intrinsic control of oesophageal EMG activity.

The effects and the sites of action of 5-Hydroxytryptamine (5HT) were examined in transverse muscular strips of pigeon oesophagus. 5-Hydroxytryptamine (0.001 to 30 microM) induced a concentration-dependent excitatory effect on the EMG activity. This response was mainly characterized by an increase in burst frequency. The maximum 5-HT-induced excitatory effect was not altered by methysergide (10 microM), but was abolished by tetrodotoxin (3 microM). Excitatory response to 5-HT was partly opposed by atropine (1 microM), potentiated by 5-methoxy-N, N-dimethyltryptamine (1 microM) and was not altered by guanethidine (10 microM). These results indicate that 5-HT activates the pigeon oesophagus indirectly via neural elements and has no direct action on the smooth muscle cells. 5-HT is thought to stimulate three different intramural neuron types: excitatory cholinergic neurons, excitatory non-cholinergic neurons and inhibitory non-cholinergic non-adrenergic neurons. The action on these different neurons seems to be mediated via different receptors.

Action Potentials↗
PubMed1985

Evidence for extrinsic control of oesophageal primary peristalsis.

The rôle of both peripheral and central mechanism in the control of primary peristalsis was studied in pigeon cervical oesophagus. The results from the transection of oesophageal muscular wall and of extrinsic nerves suggest that: primary peristalsis is programmed centrally. extrinsic motor input is carried in glossopharyngeal nerves and distributed separately at each oesophageal level through intramural neurons. intramural neurons do not seem capable of propagating the peristaltic sequence irrespective of the central control.

Animals↗