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C Blandizzi

Publications and source records attributed to C Blandizzi.

At least 55 records · Page 3Linked to original sources
PubMed1992

Atrial natriuretic peptide inhibits the spontaneous contractions of rabbit isolated ileum.

The present study investigates the effects of atriopeptin II on spontaneous phasic contractions of rabbit isolated ileum. Atriopeptin II caused a significant and concentration-dependent decrease in ileum motor activity. This effect was mimicked by 8-Br-cGMP and it was not affected by pretreatment with tetrodotoxin. Verapamil significantly decreased ileum contractions; however, in the presence of this calcium blocker, atriopeptin II further reduced ileal motility. These findings demonstrate that atriopeptin II depresses the motility of rabbit ileum through a cGMP-dependent mechanism and suggest that neither ileal neural networks nor extracellular calcium are involved in this effect.

Animals↗
PubMed1992

Gastric antisecretory effects of esaprazole in rats.

The effects of esaprazole on gastric secretion (volume, pepsin and acid output) were investigated on animal models, both in vivo and in vitro. In conscious rats whose vagal activity was stimulated by pylorus ligation, esaprazole decreased volume, acid output and pepsin secretion. In anaesthetized stomach-perfused rats, esaprazole inhibited gastric acid secretion evoked by both vagus nerve stimulation or bethanechol infusion. By contrast, on isolated guinea-pig gastric fundus, esaprazole failed to counteract the acid output stimulated by histamine, bethanechol or pentagastrin. In addition to this, phasic contractions evoked by acetylcholine on isolated guinea-pig ileum were antagonized by esaprazole only at high concentrations. The present results suggest that the inhibitory actions of esaprazole on secretory parameters involve the cholinergic parasympathetic pathway, probably through both direct and indirect mechanisms.

Acetylcholine↗
PubMed1992

[The physiopathological aspects of the atrial natriuretic factor].

The original observation by de Bold et al. (1981) of a rapid, massive, and short-lasting diuretic and natriuretic effect following injection of rat atrial extracts into intact rats, led to the identification, isolation and purification of the atrial natriuretic factor (ANF). ANF is stored in atrial myocytes and released into the blood stream by atrial distension. Available data suggest that the mechanism of ANF-induced natriuresis involves either renal hemodynamic effects, such as the increase in glomerular filtration rate and reduction of medullary tonicity, or direct effect on sodium transport in the medullary collecting ducts. ANF induces relaxation of vascular smooth muscle, decreases blood pressure and cardiac output. All these effects displayed by ANF are associated to the an inhibition of aldosterone, renin and vasopressin release. Most of these actions are mediated by specific high affinity receptors, which are coupled to a particulate guanylate cyclase. Although ANF levels are increased in some disorders, such as severe heart failure, hypertension, chronic renal failure, the role of the peptide is uncertain. To better define the potential physiopathological role and the possible therapeutic implications of this new hormonal system in conditions of disturbed body fluid and sodium homeostasis, further experimental and clinical data must be awaited.

Atrial Natriuretic Factor↗
PubMed1991

Functional evidence that acetylcholine release from Auerbach's plexus of guinea-pig ileum is modulated by alpha 2A-adrenoceptor subtype.

The effects of alpha 2-adrenoceptor ligands on electrically stimulated [3H]acetylcholine release from longitudinal muscle strips of guinea-pig ileum were examined. Xylazine or oxymetazoline reduced the release of [3H]acetylcholine in a concentration-dependent manner, both these actions being antagonized by idazoxan, CH 38083, or WB 4101. Prazosin, considered as an alpha 2B-adrenoceptor antagonist, failed to modify the inhibitory effects of xylazine or oxymetazoline. It is concluded that the alpha 2-adrenoceptors involved in the modulation of acetylcholine release from cholinergic axon terminals of guinea-pig ileum are of the alpha 2A subtype.

Acetylcholine↗
PubMed1991

Effects of quinolone carboxylic acid derivatives on GABAA receptor-mediated stimulation of gastric acid secretion and intestinal motility.

The present study investigates the effects of some quinolone carboxylic acid derivatives on GABAA receptor-mediated excitatory responses in gastrointestinal preparations in vivo and in vitro. In stomach-perfused rats, norfloxacin, nalidixic and pipemidic acid dose dependently antagonized acid hypersecretion induced by muscimol. Under the same conditions, the quinolone derivatives failed to modify acid hypersecretion evoked by 2-deoxy-D-glucose. In the isolated guinea-pig ileum, norfloxacin, nalidixic and pipemidic acid antagonized muscimol-elicited contractions in a non-competitive manner. In contrast, these drugs did not influence ileal cholinergic contractions evoked by transmural electrical stimulation or by exogenous acetylcholine. Taken together, these results suggest that the quinolone derivatives tested act as antagonists at both central and peripheral GABAA receptors. In addition, GABAA-mediated gastrointestinal responses might represent a simple and reliable method to assay the GABAA receptor antagonist properties of new quinolone derivatives.

Acetylcholine↗
PubMed1991

Phaclofen-sensitive GABA-B receptors do not mediate excitatory effects of baclofen on gastric secretion.

The present study investigates the effects of centrally or peripherally administered baclofen on gastric acid secretion from pylorus-ligated rats. The influence of baclofen on basal acid secretion from isolated guinea-pig gastric fundus was also evaluated. At all doses employed, intracerebroventricular baclofen significantly decreased acid secretion, this inhibitory action being antagonized by intracerebroventricular phaclofen. Intravenous baclofen induced both gastric inhibitory and excitatory responses at low and high doses, respectively. Intracerebroventricular phaclofen prevented the inhibitory effect, while neither intracerebroventricular nor intravenous phaclofen modified the stimulant action of parenteral baclofen. Both central and parenteral muscimol did not influence gastric acid secretion. Moreover, baclofen or muscimol were without effect on basal acid secretion from isolated guinea-pig gastric fundus, whereas bethanechol caused a marked and concentration-dependent stimulant action. The present results provide further evidence for the inhibitory role of central phaclofen-sensitive GABA-B receptors in the regulation of acid secretion. In addition they indicate that the hypersecretory effect exerted by parenteral baclofen may depend upon the activation of putative peripheral non-A and phaclofen-insensitive GABA-B receptors. Finally, peripheral GABA receptors do not appear to be significantly involved in the direct control of gastric secretion.

Animals↗
PubMed1991

[The clinical efficacy of roxithromycin in patients with acute odontogenic infections].

The clinical efficacy of a macrolide antibiotic, roxithromycin, was evaluated in 24 patients affected by acute odontogenic infections. Patients were treated with a first dose of 300 mg p.o. which was followed by 150 mg p.o. 12-hourly for the following two days. Total responses were evaluated by an arbitrary scale. The results showed that an excellent and good response was obtained in 99.96% of treated patients. On the basis of clinically compared data and the drug safety it may be concluded that roxithromycin can be successfully used in the treatment of odontogenic infections.

Acute Disease↗
PubMed1990

Central GABAA excitatory and GABAB inhibitory receptors regulate gastric acid secretion in rats.

The present study investigates the effects of GABAA- and GABAB-receptor agonists and antagonists on gastric secretion after their i.c.v. administration to conscious pylorus-ligated rats and anaesthetized stomach lumen-perfused rats. Muscimol was without effect in pylorus-ligated rats, whereas baclofen produced a significant decrease in acid secretion, which was fully prevented by phaclofen. Under these conditions, a significant decrease in acid secretion was also obtained with bicuculline. In stomach lumen-perfused rats, muscimol caused a marked, dose-dependent increase in acid secretion, which was antagonized by bicuculline. Under the same conditions, baclofen induced a moderate, but significant, bicuculline-sensitive increase in acid secretion. Overall, our results suggest the presence of two central GABA pathways which mediate opposite effects: (a) a bicuculline-sensitive GABAA-receptor, the stimulation of which increases acid secretion under pharmacological depression of central vagal tone (anaesthetized rats); (b) a phaclofen-sensitive GABAB-receptor, the activation of which decreases vagally stimulated acid secretion (pylorus-ligated rats).

Anesthesia↗
PubMed1990

Modulation of gastric acid secretion by peripheral presynaptic alpha 2-adrenoceptors at both sympathetic and parasympathetic pathways.

1. The effects of the alpha 2-adrenoceptor agonist detomidine, and the antagonists idazoxan and CH-38083 were examined on gastric acid secretion from non-vagotomized and vagotomized stomach lumen-perfused rats. The effects of detomidine on acid secretion from isolated guinea-pig gastric fundus were also evaluated. 2. In both non-vagotomized and vagotomized rats i.p. administration of detomidine significantly increased acid secretion, whereas i.c.v. detomidine was without effect. The stimulant action of i.p. detomidine was antagonized by both i.p. idazoxan and CH-38083 as well as by pretreatment with reserpine. 3. In vagotomized and reserpinized rats whose acid secretion was increased by electrical stimulation of the left vagus nerve, i.p. injection of detomidine caused inhibitory effects on acid secretion which were fully antagonized by both i.p. idazoxan and CH-38083. 4. Both idazoxan and CH-38083 caused a significant increase in acid secretion induced by vagal stimulation. At higher doses the two antagonists displayed a potentiating effect on vagally induced acid secretion only when they were associated to i.v. infusion of prazosin and propranolol. 5. Detomidine was without effect on acid secretion from isolated guinea-pig gastric fundus, whereas histamine or bethanechol caused a marked and dose-dependent stimulant action. 6. Overall, these results provide evidence that peripheral presynaptic alpha 2-adrenoceptors modulate both adrenergic inhibitory and cholinergic excitatory influences on rat gastric acid secretion.

Adrenergic alpha-Antagonists↗
PubMed1990

Alpha 2-adrenoceptor-mediated inhibitory and excitatory effects of detomidine on rat gastric acid secretion.

The effects of the selective alpha 2-adrenoceptor agonist detomidine on gastric acid secretion from pylorus-ligated and stomach-perfused rats have been investigated. In pylorus-ligated rats i.p. injection of detomidine markedly inhibited acid secretion, this effect being prevented by yohimbine or idazoxan. Under the same conditions, idazoxan significantly increased secretion in a dose-independent fashion. In non-vagotomized and vagotomized stomach-perfused rats i.p. detomidine stimulated acid secretion: this excitatory effect was antagonized by idazoxan. The present results suggest that both inhibitory and excitatory gastric secretory effects of detomidine are mediated by alpha 2-adrenoceptors on cholinergic and adrenergic nerves, respectively. The stimulant activity of idazoxan on gastric secretion from pylorus-ligated rats may be interpreted in terms of increased excitatory vagal tone following the blockade of inhibitory alpha 2-adrenoceptors.

Adrenergic alpha-Agonists↗
PubMed1990

Differential affinities of AF-DX 116, atropine and pirenzepine for muscarinic receptors of guinea pig gastric fundus, atria and urinary bladder: might atropine distinguish among muscarinic receptor subtypes?

The pA2 values and the Schild plots of the antimuscarinic drugs AF-DX 116, atropine and pirenzepine for muscarinic receptors of isolated guinea pig gastric fundus (acid secretion) and atrial and urinary bladder preparations (contractile force) obtained from the same animals were calculated against bethanechol as the agonist. The antimuscarinic drugs concentration-dependently shifted the concentration-response curves to bethanechol to the right without any change in the maximum response. The analysis of data based on Schild plots was consistent with a simple competitive antagonism, since regression slopes did not differ significantly from unity. The pA2 values indicated a significantly higher affinity of AF-DX 116 and atropine for atrial muscarinic receptors with respect to those of the gastric mucosa or urinary bladder. By contrast, in the case of pirenzepine the pA2 values for the three tissues did not differ significantly. These results suggest that each examined tissue apparently contains homogeneous population of acetylcholine muscarinic (M2) receptors. The pA2 values found for AF-DX 116 and atropine suggest, however, that the putative M2 subtype of atrial muscarinic receptor differs from both those of the gastric fundus and those of the urinary bladder.

Animals↗
PubMed1989

GABA-A-mediated gastrin release induced by baclofen in the isolated vascularly perfused rat stomach.

In order to investigate the role of peripheral GABA-B receptors, the effects of the putative GABA-B agonist baclofen on immunoreactive gastrin release from an isolated vascularly perfused rat stomach preparation were examined. The vascular infusion of baclofen at graded concentrations induced a dose-dependent increase in gastrin release; this was unaffected by the GABA-B antagonist delta-aminovaleric acid, but was fully prevented by the selective GABA-A antagonist bicuculline as well as by atropine or tetrodotoxin. These results suggest that the stimulant effects of baclofen are mediated by nervous cholinergic structures associated with GABA-A receptors, and indicate that this GABA-B agonist must be regarded as a partial agonist of peripheral GABA-A receptors.

Amino Acids↗
PubMed1988

Excitatory and inhibitory cholinergic effects of yohimbine on isolated guinea-pig small intestine.

The interaction of yohimbine with the cholinergic intestinal system was investigated in the isolated guinea-pig ileum using a wide range of drug concentrations from 3 x 10(-13) to 2 x 10(-4) g/ml. Low concentrations of yohimbine (3 x 10(-13) to 3 x 10(-11) g/ml) caused dose-dependent contractions of the ileal longitudinal muscle, which were potentiated by eserine 1 x 10(-8) g/ml and prevented by tetrodotoxin 1 x 10(-6) g/ml or by atropine 1 x 10(-12) g/ml; methysergide and diphenydramine were ineffective up to 3 x 10(-7) g/ml dose. Submaximal stimulatory responses evoked by twitch stimulation or by acetylcholine were significantly potentiated by the same concentrations of yohimbine (3 x 10(-13) to 3 x 10(-11) g/ml) and blocked by atropine 1 x 10(-12) g/ml. By contrast, high concentrations of yohimbine (1 x 10(-6) to 2 x 10(-4) g/ml) displayed dose-dependent inhibitory effects on cholinergic responses. The stimulant effect of yohimbine seems to be indirect and mediated by the increase in the release of acetylcholine, while the inhibitory action may be due to a molecular interaction with the muscarinic receptors allowing non-specific receptor blockade.

Acetylcholine↗
PubMedDate not supplied

Central alpha-2 adrenoceptors regulate central and peripheral functions.

Central alpha-2 adrenoceptors regulate a variety of functions including blood pressure, gastrointestinal activity, hormonal secretion, sleep-waking cycle, analgesia, anxiety and some aspects of the withdrawal reaction to opioids. Evidence has been provided that clonidine decreases blood pressure, inhibits salivary secretion and reduces gastrointestinal secretion and motility. Several alpha-2 adrenoceptor agonists reduce wakefulness and inhibit paradoxical sleep, whereas novel imidazoline derivatives, such as detomidine, display sedative and analgesic properties which have been related to the activation of central alpha-2 adrenoceptors. Recent data emphasize the importance of somatodendritic alpha-2 autoreceptors compared to presynaptic alpha-2 autoreceptors as physiological modulators of noradrenergic activity in the central nervous system. In addition, increasing experimental evidence has been provided on the relevant role played by central alpha-2 heteroreceptors (presynaptic and somatodendritic) in the regulation of several functions. Some effects mediated by the activation of alpha-2 adrenoceptors are very similar to those following stimulation of mu opioid receptors. This parallelism can be explained, at least in part, by the presence of these receptors on the same neurons on which they exert an inhibitory action mediated by the same cellular mechanisms. This review resumés the most prominent data about the role played by central alpha-2 adrenoceptors in the regulation of overall functions.

Animals↗
PubMedDate not supplied

Gastroprotective effects of pantoprazole against experimental mucosal damage.

The present study investigated the gastroprotective effects of the proton pump inhibitor pantoprazole on gastric mucosal damage induced by ethanol-HCl in rats. Omeprazole was used as reference drug. The morphometric analysis of gastric histological sections revealed that pantoprazole and omeprazole dose-dependently prevented the necrotic mucosal injury evoked by ethanol-HCl (ED50 = 14.1 and 21.6 micromol/kg, respectively). These effects were associated with a marked increment of Alcian blue recovery from gastric bound mucus (ED50 = 18.8 and 29.3 micromol/kg, respectively). In addition, both pantoprazole and omeprazole inhibited gastric acid secretion in pylorus-ligated rats (ED50 = 1.5 and 3.3 micromol/kg, respectively). Further experiments indicated that the protective effects of pantoprazole were not modified by L-365,260 (a gastrin receptor antagonist), suramin (a drug able to interfere with endogenous growth factors), N(G)-nitro-L-arginine (an inhibitor of nitric oxide synthase) or systemic ablation of capsaicin-sensitive sensory nerves, whereas they were partly blocked by indomethacin (an inhibitor of prostaglandin synthesis) and fully prevented by N-ethylmaleimide (a potent blocker of sulfhydryl compounds). The present data provide histomorphometric evidence that: 1) pantoprazole is endowed with gastroprotective properties and is more active than omeprazole in preventing the necrotic mucosal damage induced by ethanol-HCl; 2) according to the rank order of ED50 values, the protective effects of both drugs appear to depend mainly on the enhancement of the gastric mucosal barrier rather than on the inhibition of acid secretion; 3) an increased production of prostaglandins, as well as an increased availability of sulfhydryl radicals at the level of the gastric mucosa may account for the gastroprotective effects of pantoprazole.

2-Pyridinylmethylsulfinylbenzimidazoles↗