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Biomedical subjects

R Serio

Publications and source records attributed to R Serio.

At least 37 records · Page 2Linked to original sources
PubMed1995

Motility pattern of isolated rat proximal colon and excitatory action of neurotensin.

The investigation concerned the effects of neurotensin on mechanical activity of isolated rat proximal colon. An isometric-isovolumic preparation was used. Colonic segments showed spontaneous contractile activity, consisting of regular changes in both endoluminal and isometric tension. Neurotensin (1 pM to 0.1 microM) induced a concentration-dependent tonic contraction of both circular and longitudinal muscle accompanied by high frequency oscillatory activity. Desensitization of the neurotensin receptors antagonized the contractile activity of neurotensin. The excitatory effects of neurotensin were partially blocked to the same degree by tetrodotoxin and atropine, indicating that a component of the neurotensin-mediated contraction involves the release of endogenous acetylcholine. The tetrodotoxin-resistant component of the neurotensin-induced effect seems to be due to a direct action on the smooth muscle cells.

Acetylcholine↗
PubMed1995

Nitric oxide is involved in non-adrenergic, non-cholinergic inhibitory neurotransmission in rat duodenum.

1. In rat duodenum, electrical field stimulation (EFS) induced a relaxation due to activation of non-adrenergic, non-cholinergic (NANC) inhibitory intramural neurones. 2. Nitric oxide synthase (NOS) inhibitors, N omega-nitro-L-arginine (L-NNA) and N omega-nitro-L-arginine methyl ester (L-NAME), caused a dose-dependent reduction in amplitude of the NANC relaxation. Responses to low frequencies of stimulation were more sensitive to NOS inhibitors than those to high frequencies. 3. Effects induced by NOS inhibitors were stereospecific since D-NNA and D-NAME did not affect NANC relaxation. L-arginine, but not D-arginine, partially prevented the effects induced by NOS inhibitors on NANC relaxation. 4. The nitrovasodilator drug, sodium nitroprusside, caused muscle relaxation which was not affected by preincubation with either tetrodotoxin (TTX), L-NNA or L-NAME. 5. alpha-Chymotrypsin reduced relaxations elicited by stimulation of NANC nerves, especially when high frequencies of stimulation were used. The residual NANC relaxation was further reduced by NOS inhibitors. In the same way, alpha-chymotrypsin was able to further reduce the relaxation observed after NOS inhibitors. 6. These results suggest that nitric oxide (NO) and a peptide are involved in NANC relaxation of rat duodenal smooth muscle. NO and peptidergic pathways act in parallel to produce muscle relaxation and they are preferentially activated by stimuli at low and high frequencies, respectively.

Amino Acid Oxidoreductases↗
PubMed1995

Nonadrenergic, noncholinergic inhibitory junction potentials in rat proximal colon: role of nitric oxide.

Using a single sucrose gap apparatus, experiments were performed to determine the involvement of nitric oxide (NO) in the generation of nonadrenergic, noncholinergic (NANC) inhibitory junction potentials in circular muscle of rat proximal colon. Inhibitors of NO synthase, N omega-nitro-L-arginine and its methyl ester, reduced the amplitude of the electrically evoked inhibitory junction potentials, without affecting membrane resting potential. Such an effect was stereospecific and it was prevented by L-arginine but not by D-arginine. Sodium nitroprusside induced a tetrodotoxin-resistant hyperpolarization, which was not affected by NO synthase inhibitors. Apamin reduced sodium nitroprusside induced hyperpolarization, as well as NANC inhibitory junction potentials, and alpha-chymotrypsin decreased the amplitude of electrical field stimulation evoked responses. Residual responses after NO synthase inhibitors or after alpha-chymotrypsin were further reduced by pretreatment with alpha-chymotrypsin or NO synthase inhibitors, respectively. These results suggest that, in rat colonic circular muscle, NO plays an important role in NANC inhibitory junction potential generation. However, another mechanism, peptidergic in nature, is also involved.

Animals↗
PubMed1993

Modulation of non-adrenergic non-cholinergic inhibitory transmission in rat duodenum: role of opiates and 5-hydroxytryptamine.

In rat duodenal segments in vitro, electrical field stimulation induced a TTX-sensitive relaxation in the presence of atropine and guanethidine. A correlation between the amplitude of the evoked response and stimulus frequency was observed. Opioid peptides DAGO, DPDPE and DYN caused a dose-dependent increase in the amplitude of the response to EFS. Naloxone shifted to the right the dose-response curves for each opioid peptide significantly enhancing the ED50 values. The amplitude of the response to EFS was enhanced, dose-dependently, also in the presence of 5-HT. Such an effect induced by 5-HT was prevented by 5-HT receptor desensitization, but persisted unchanged after naloxone pretreatment. Opioids failed to affect the response to EFS after 5-HT receptor desensitization. Results suggest that in rat duodenum opioids modulate NANC inhibitory neurotransmission, indirectly the release of 5-HT.

Analgesics↗
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

Excitatory effects of opiates on the spontaneous EMG activity in pigeon oesophagus.

The effects and the mechanism of action of morphine, methionine-enkephalin and leucine-enkephalin were examined in transverse muscular strips from pigeon oesophagus. All the opiates produced a concentration-dependent excitatory effect on the spontaneous EMG activity, characterized mainly by an increase in the spike burst frequency. The maximal excitatory response to morphine and opioid peptides was fully antagonized by naloxone and tetrodotoxin, significantly reduced by atropine and it was not affected by guanethidine pretreatment. Treatment of pigeons with reserpine abolished the excitatory effects induced by opiates. The above results suggest the existence of specific opioid receptors in pigeon oesophagus. Opiates have no direct action on smooth muscle cells, increasing the EMG activity via excitatory both cholinergic and non-adrenergic non-cholinergic neurons. The hypothesis of a possible involvement of serotonergic interneurons might be advanced.

Animals↗