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Biomedical subjects

A Badia

Publications and source records attributed to A Badia.

At least 73 records · Page 4Linked to original sources
PubMed1992

Post-train administration of 9-amino-1,2,3,4-tetrahydroacridine enhances passive avoidance retention and decreases beta-adrenoceptor-linked cyclic AMP formation in middle-aged rats.

The possible involvement of beta-adrenoceptor system in the effectiveness of 9-amino-1,2,3,4-tetrahydroacridine (THA) to attenuate retention deficits exhibited by middle-aged rats in a one-trial passive avoidance task has been investigated. THA (2.5 mg.kg-1), injected i.p. after training, induced a significant increase in test step-through latency (STL) in middle-aged rats. Post-training injection of THA reduced basal and isoprenaline stimulated cyclic AMP accumulation in cortex and hippocampus of every group of rats. It is suggested that the effect of THA on memory processes may involve an action on beta-adrenoceptor-linked cyclic AMP accumulation.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Acute effects of tetrahydroaminoacridine on beta-adrenoceptor-linked cyclic AMP accumulation in brain of young and middle-aged rats.

The effects of acute treatment with 1,2,3,4-tetrahydro-9-aminoacridine (THA), a 4-aminopyridine derivative clinically effective in Alzheimer's disease, on beta-adrenoceptor-linked cyclic AMP accumulation have been investigated in cortical and hippocampal structures of young and middle-aged rats. In a first series of experiments, pretreatment with 2.5 mg/kg THA decreased basal cyclic AMP accumulation. When a phosphodiesterase inhibitor was added to the preparation, THA again decreased cyclic AMP levels in young rats, but failed to significantly modify cyclic AMP accumulation in middle-aged animals. Finally, in isoprenaline-stimulated conditions, acute treatment with tacrine was able to diminish cyclic AMP accumulation in every group of rats. It is suggested that the neurochemical action of THA in mammalian brain is more complex than earlier has been anticipated and may involve an action on beta-adrenoceptors.

1-Methyl-3-isobutylxanthine↗
PubMed1991

Dietary factors and stomach cancer in Spain: a multi-centre case-control study.

A multi-centre case-control study of diet and gastric cancer was carried out in 4 regions of Spain (Aragon, Castile, Catalonia and Galicia). We selected 354 cases of pathologically confirmed gastric adenocarcinoma from 15 hospitals, representative of nearly all those in the study areas. A control for each case, matched by age, sex and area of residence, was selected from the same hospital as the case. Habitual diet was investigated by the dietary history method, and past diet by means of a frequency questionnaire. The results regarding consumption of food items are presented here. With respect to habitual diet, an increase in risk was associated with consumption of preserved fish, cold cuts and oleaginous fruits. A high intake of cooked green vegetables, fresh noncitrus fruit and dried fruit showed an inverse association with the risk of gastric cancer. Simultaneous intake of 2 groups of food which increase or decrease the risk of cancer strengthens the respective individual effect. The intake of protective food items seems to neutralize the effects of food items which increase risk. With reference to past diet, a possible protective effect was observed for daily consumption of fresh fruit and green vegetables.

Adenocarcinoma↗
PubMed1991

Mechanisms underlying the differential sensitivity to alpha 1-adrenoceptor activation in the bisected rat vas deferens.

1. The factors underlying the different responsiveness of the prostatic and epididymal portions of rat vas deferens to alpha 1-adrenoceptor stimulation were investigated. 2. The alpha 1-adrenoceptors in membranes of both halves of rat vas deferens were labelled with [3H]-prazosin and the affinities of agonists and antagonists for these receptors were determined. In saturation studies, the Bmax and KD values for [3H]-prazosin in membranes of both portions were the same. 3. In competition studies, the inhibition curves for phentolamine were biphasic and consistent with the presence of both alpha 1a- and alpha 1b-adrenoceptor subtypes. The proportions of binding sites with high and low affinity for phentolamine in both halves of rat vas deferens were similar and in good agreement with the percentages of binding sites for WB-4101 and phentolamine previously reported in the whole rat vas deferens. 4. The phenylethylamines displaced [3H]-prazosin with a shallow inhibition curve. The data are compatible with the assumption of two affinity states for the binding sites. For the imidazoline compounds no such distinct affinity states could be demonstrated. 5. The affinity for, and the relative intrinsic efficacy on postsynaptic alpha 1-adrenoceptors of both portions of rat vas deferens were studied for noradrenaline, phenylephrine and methoxamine by irreversible inactivation of the alpha 1-adrenoceptors by phenoxybenzamine. The parameters for partial agonists were determined by comparing the responses to the partial agonist to those of a full agonist in the same tissue. Homogeneous estimates of the equilibrium dissociation constants (Ka) were obtained, indicating that these agonists bind to the receptors of both tissues in an identical manner. Further, estimation of the intrinsic efficacy of agonists relative to noradrenaline, indicated no differences between the two halves of rat vas deferens. 6. Ka values for agonist activation of the functional alpha 1-adrenoceptors were compared with K, values for agonist inhibition of specific [3H]-prazosin binding. The K. values were well correlated with the low affinity K, values for phenylethylamines in both portions of rat vas deferens, suggesting that the initial event in signal transduction by alpha 1,-adrenoceptors is the binding to the low affinity state of the receptor. 7. There was a non-linear relationship between response and receptor occupancy in both halves of rat vas deferens but the occupancy-response coupling was more efficient in the epididymal than in the prostatic portion. This fact may account for the differences observed in the functional responses.

Adrenergic alpha-Agonists↗
PubMed1990

Paraxanthine displaces the binding of [3H]SCH 23390 from rat striatal membranes.

We present evidence showing that paraxanthine (1,7-dimethylxanthine), the main metabolite of caffeine in man, displaces the binding of [3H]SCH 23390, a radioligand which selectively labels dopamine D-1 receptors when used at low concentrations, from striatal membranes of the rat. The displacement was competitive and indicated the existence of two affinity states (Hill coefficient = 0.49; K(high) = 0.15 microM; K(low) = 95.9 microM, %R(high) = 32.4). When the stable GTP analog Gpp(NH)p was included, the displacement curve indicated the presence of only the low-affinity state (Hill coefficient = 1.16; Ki = 72.1 microM). However, paraxanthine did not displace the specific binding of [3H]spiperone. After injection of 30 mg/kg s.c. of caffeine, a maximum of 10 microM of paraxanthine was found in striatal homogenates, which could be sufficient to occupy dopamine D-1 receptors. Our results suggest that a dopaminergic action of paraxanthine could be involved in the behavioural stimulation produced by caffeine.

Animals↗
PubMed1990

Effects of chronic antidepressant treatment on alpha 1- and alpha 2-adrenoceptors in the rat anococcygeus muscle.

The effects of a single administration (48 hours) and of chronic (14 days) treatment with tricyclic (desipramine, nortryptiline) and nontricyclic (mianserin, nomifensine) antidepressant drugs on responses of the isolated anococcygeus muscle to the alpha 2-adrenoceptor agonist xylazine (inhibition of contraction to field stimulation at 1 Hz) and to the alpha 1-adrenoceptor agonist phenylephrine (contraction of the muscle) have been studied. Of the drugs used only desipramine and nortryptiline administered chronically reduced the responsiveness of the anococcygeus muscle to phenylephrine suggesting a desensitization of postsynaptic alpha 1-adrenoceptors. Long-term but not acute administration of antidepressants resulted in significant decrease in sensitivity of presynaptic alpha 2-adrenoceptors to xylazine. These results show that the adaptative changes of alpha-adrenoceptors in the rat anococcygeus muscle following long-term administration may depend on the efficiency to inhibit the neuronal uptake and the ability to antagonize alpha 1-adrenoceptors.

Animals↗
PubMed1990

Influence of extracellular calcium in the effects of dibekacin and diltiazem on indirectly elicited tetanic responses in the rat phrenic-hemidiaphragm preparation.

1. Dibekacin (70 microM-3 mM) produced a decrease of peak tetanic tension in a concentration-dependent manner and this effect was dependent on extracellular calcium (0.3-2.5 mM Ca2+). Only minimal fade was observed and it was not related with extracellular calcium concentrations. 2. Diltiazem (30-300 microM) decreased peak tetanic tension and produced tetanic fade. Both effects were independent of extracellular calcium, although a significant potentiation was observed at 0.3 mM calcium. 3. It is concluded that tetanic parameters are related differently to extracellular calcium.

Animals↗
PubMed1989

Differential effects of chronic treatment with mianserin and protryptiline on rat brain cortical alpha 1-adrenoceptors.

Chronic administration of mianserin induced an increase in the density of [3H] prazosin binding sites (23%) in membranes and in the maximal noradrenaline stimulation of phosphoinositide breakdown (81%) in slices from rat brain cortex. In contrast, a similar treatment with protryptiline did not induce any significant changes. These findings suggest that the effects of antidepressant drugs on rat brain cortical alpha 1-adrenoceptors may depend on the characteristics of the drug used.

Animals↗
PubMed1989

Increased peripheral alpha 1-adrenoceptor sensitivity following chronic thioridazine treatment in the pithed rat.

The effect of chronic treatment (10 days) with thioridazine (25 mg/kg per day, i.p.) on the increase in diastolic blood pressure induced by methoxamine and xylazine was studied in the pithed rat. The dose-response curve for methoxamine, but not for xylazine, was shifted to the left by the neuroleptic. These results indicate that postjunctional alpha 1-adrenoceptors in the rat blood vessels become supersensitive after long-term treatment with thioridazine.

Animals↗
PubMed1989

Blocking effect of diltiazem in the isolated rat phrenic hemidiaphragm.

The effects of diltiazem on indirectly and directly elicited twitch were studied in the isolated rat phrenic hemidiaphragm preparation. Diltiazem (30-500 microM) blocked the indirectly elicited twitch response and this effect was not affected by reducing the extracellular calcium from 2.5 to 1.25 mM. An effect on the directly elicited twitch was also observed (100-300 microM). Diltiazem (30-300 microM) blocked the peak tetanic tension and tetanic fade was present. The results were consistent with an action of diltiazem on the nicotinic receptor-ion channel complex.

Animals↗
PubMed1989

The neuromuscular blocking effect of dibekacin and its reversal by Ca2+ and drugs in the isolated rat phrenic-hemidiaphragm preparation.

1. Dibekacin (0.3-3 mM) reduced indirectly elicited twitches in rat phrenic-hemidiaphragm. This effect was potentiated in low extracellular calcium media. 2. The blockade induced by dibekacin (3 mM) could be reversed by calcium (2.5 mM), 3,4-diamino-pyridine (3,4-DAP, 10 microM) or guanidine (3 mM), whereas neostigmine (3 microM), eserine (25 microM) or tetraethylammonium (100 microM) were less potent. 3. Dibekacin (3 mM) blocked directly-elicited twitches. Low concentrations were unable to obtain any effect. 4. It is concluded that dibekacin exerts its blocking action by limiting the calcium entry at motor nerve terminals, but a postsynaptic effect is also present. 3,4-DAP, guanidine and calcium were the most potent drugs in reversing the blockade.

Animals↗
PubMed1989

Effects of some antipsychotic drugs on cardiovascular catecholamine receptors in the rat.

1. Experiments were performed to determine the activity of four antipsychotic drugs on several catecholamine receptors that control the sympathetic cardiovascular responses in rats. 2. Chlorpromazine, thioridazine (0.03 and 0.1 mg kg-1) and haloperidol (0.3 and 1 mg kg-1) inhibited methoxamine-induced diastolic blood pressure increases in the pithed rat, whereas sulpiride (1 and 3 mg kg-1) was without effect. 3. Only sulpiride (3 mg kg-1) antagonized the pressor responses induced by xylazine. 4. Xylazine inhibited the heart rate increase induced by electrical stimulation of the spinal cord (C7-Th1) in the pithed rat. This effect was partially prevented by sulpiride (1 and 3 mg kg-1) and chlorpromazine (0.3 mg kg-1). A higher dose of chlorpromazine (1 mg kg-1) abolished the inhibitory effect of xylazine. 5. Apomorphine infusion inhibited the pressor responses induced by electrical stimulation (Th5-L4) in pithed rats. This effect was reversed by sulpiride (0.01, 0.03 and 0.1 mg kg-1) and partially antagonized by haloperidol (0.1 mg kg-1). 6. The depressor response to fenoldopam in anaesthetized rats was only inhibited by the higher dose of chlorpromazine and thioridazine (3 mg kg-1). 7. Our results suggest that, in the peripheral nervous system of the rat, haloperidol and sulpiride act as antagonists of DA2 receptors while chlorpromazine and thioridazine antagonized DA1 receptors. Furthermore, thioridazine and haloperidol show alpha 1-adrenoreceptor antagonist properties, whereas sulpiride antagonizes alpha 2-adrenoreceptors. Chlorpromazine shows mixed alpha 1/alpha 2-adrenoreceptor antagonism.

Animals↗
PubMed1989

Effects of St-587 on the alpha-adrenoceptors in the bisected rat vas deferens.

The effects of the alpha-adrenoceptor agonist St-587 have been studied on the twitch responses induced by field stimulation in the prostatic portion of rat vas deferens. Moreover the drug's influence on the unstimulated prostatic and epididymal halves of rat vas deferens has also been determined. Alone and after addition of yohimbine (0.3 microM) it enhanced in a concentration-dependent manner the twitch responses in the prostatic half. Prazosin competitively antagonized (pA2 = 8.41 +/- 0.03) this effect. The enhancing effect of St-587 was not reduced in reserpinized animals. These results suggest that post-synaptic alpha 1-adrenoceptors are involved in the potentiation of twitch responses induced by St-587. When alpha 1-adrenoceptors were blocked by prazosin (0.1 microM), St-587 partially inhibited the twitch responses of the prostatic portion of rat vas deferens (Emax = 49.5 +/- 3.5%). Yohimbine completely reversed the inhibitory effects of both St-587 and clonidine. Furthermore St-587 antagonized the inhibitory effects of clonidine on twitch responses. Thus it appears that St-587 also behaves as a partial agonist of presynaptic alpha 2-adrenoceptors in this portion of rat vas deferens, but it did not induce contractions in the unstimulated prostatic half of the vas deferens. However, it competitively antagonized the alpha 1-adrenoceptor agonist phenylephrine by acting as an antagonist of prostatic postsynaptic alpha 1 adrenoceptors. These alpha 1-adrenoceptors are probably different from those that mediate the twitch enhancing response to St-587 in that portion. On the other hand, St-587 was a partial agonist of alpha 1-adrenoceptors in the epididymal half.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1988

Effects of ergotamine on cardiovascular catecholamine receptors in the pithed rat.

1. Ergotamine (3-10 micrograms/kg) inhibited the electrical stimulation-induced pressor and cardiac responses without modifying pressor responses of noradrenaline and tyramine in the pithed rat. 2. Yohimbine (0.3 mg/kg) partially prevented the ergotamine cardiac and vascular inhibitory effects but sulpiride (0.3 mg/kg) only prevented it at vascular level. Both antagonists together abolished the ergotamine inhibition of electrical stimulation-induced pressor responses. 3. The cumulative dose-response curve of ergotamine (1-100 micrograms/kg) vasoconstrictor effects was partially inhibited to the same extent by prazosin (1 mg/kg) and yohimbine (0.3 mg/kg). A greater inhibition was observed with both antagonists administered together. 4. Ergotamine (30 micrograms/kg), in presence of yohimbine, inhibited the pressor responses of methoxamine, without any effect on xylazine pressor responses. 5. These data indicate that ergotamine acts as an agonist of both the presynaptic dopamine receptors and alpha 2-adrenoceptors, of alpha 1 and alpha 2-postsynaptic adrenoceptors, and also as an antagonist of the postsynaptic alpha 1-adrenoceptors.

Animals↗
PubMed1986

Presynaptic actions of piribedil on the cardiovascular system of the pithed rat.

The influence of piribedil on cardiovascular sympathetic responses has been studied in the pithed rat. Piribedil (0.3-1 mg kg-1) inhibited the increases of diastolic blood pressure induced by spinal cord electrical stimulation at the level Th5-L4. This effect was reversed by sulpiride (0.3 mg kg-1) but not by yohimbine (0.3 mg kg-1). The cardiovascular responses induced by noradrenaline were unaffected by piribedil (0.3-1 mg kg-1). However piribedil (0.3-1 mg kg-1) did not modify the heart rate increase induced by spinal cord electrical stimulation at the C7-Th1 level. These results suggest that piribedil inhibits the vascular sympathetic transmission in the pithed rat via stimulation of presynaptic dopamine receptors.

Animals↗
PubMed1985

Effects of bromocriptine on catecholamine receptors mediating cardiovascular responses in the pithed rat.

The interaction of bromocriptine with several catecholamine receptors that control the sympathetic responses at cardiac and vascular level has been studied in pithed adrenalectomized and vagotomized normotensive rats. Bromocriptine (30 and 100 micrograms/kg) inhibited the stimulation-induced pressor responses in the pithed rat without modifying the pressor responses induced by noradrenaline. Sulpiride (0.3 mg/kg) abolished the effects of bromocriptine (30 micrograms/kg) but only partially prevented the effects of bromocriptine (100 micrograms/kg) on the stimulation-induced pressor responses. Yohimbine (0.3 mg/kg) partially antagonised the inhibitory effect of bromocriptine on stimulation-induced pressor responses. Combination of yohimbine and sulpiride abolished attenuation of the stimulation-induced pressor responses by bromocriptine (100 micrograms/kg). Bromocriptine (0.3 and 1 mg/kg) shifted to the right the frequency-response curve of increases in heart rate. This effect was prevented by yohimbine (0.3 mg/kg) but not by sulpiride (0.3 mg/kg). The same doses of bromocriptine were ineffective on heart rate increases induced by noradrenaline. Bromocriptine (0.3 and 1 mg/kg) shifted to the right the increases in diastolic blood pressure induced by methoxamine without modifying those induced by xylazine and noradrenaline. These results suggest that bromocriptine acts on the peripheral sympathetic nervous system of the pithed rat as an agonist of presynaptic dopamine receptors and alpha 2-adrenoreceptors and as an antagonist of postsynaptic alpha 1-adrenoreceptors.

Animals↗