Browsing by Author "MIRANDA, H"

Now showing 1 - 12 of 12
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    ANDROGENS AND EFFECTS OF OPIOIDS AND CATECHOLAMINES ON THE SMOOTH-MUSCLE OF THE RAT VAS-DEFERENS
    (1985) MIRANDA, H; PEREZ, E; FERNANDEZ, E; ROSSELOT, F; VERGARA, JF; WOLSTENHOLME, WW; ZUAZO, A
    In the neuronal electrically stimulated vas deferens of the rat, the responses evoked by morphine, .beta.-endorphin and catecholamines were studied. The tissue was obtained from rats at various times (7-60 days) following castration, adrenalectomy and castration with adrenalectomy. Pharmacological data are presented which verify an increased responsiveness to morphine after castration with or without adrenalectomy. Decreased responsiveness was observed after adrenalectomy alone. Decreased responsiveness of the vas deferens to catecholamines was observed after castration, adrenalectomy and castration with adrenalectomy. Since the responsiveness of the electrically stimulated vas deferens to .beta.-endorphin was unchanged by this treatment (castration, adrenalectomy), the .epsilon.-opioid receptor may be unaffected by androgens.
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    BIOGENIC-AMINES AND BETA-ENDORPHIN RESPONSES IN THE RAT VAS-DEFERENS
    (1982) MIRANDA, H; VERGARA, JF; ROSSELOT, F; FERNANDEZ, E
    Activation of opioid peptide receptors by .beta.-endorphin results in a change of bioamines in peripheral tissues. The action of .beta.-endorphin on the smooth muscle of the isolated rat vas deferens may be independent of catecholaminergic, cholinergic and tryptaminergic neurotransmission. The action may involve a specific opioid .epsilon.-receptor having a high degree of affinity for .beta.-endorphin.
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    CHOLINERGIC TRANSMISSION IN VAS-DEFERENS
    (1983) BUSTOS, E; MIRANDA, H; PAEILE, C
    Prazosin, haloperidol, propranolol or timolol had no effect on the electrically evoked muscular twitch. Atropine was able to antagonize competitively acetylcholine (pA2 = 9.29 .+-. 0.30). The muscular twitch of the Octodon degus vas deferens was only partially abolished by atropine (53.2 .+-. 0.72). The present results can be interpreted assuming that the O. degus vas deferens has one component muscarinic in its innervation.
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    DEVELOPMENT OF TOLERANCE TO THE EXCITATORY EFFECT OF MORPHINE AND CROSS-TOLERANCE TO THE INHIBITORY-ACTION OF BETA-ENDORPHIN IN THE ISOLATED RAT VAS-DEFERENS
    (1981) HUIDOBROTORO, JP; MIRANDA, H; HUIDOBRO, F
    In the isolated rat vas deferens, morphine caused an increase in the neuromuscular twitch evoked by electrical stimulation. In rats chronically treated with morphine, the concentration of the opiate required to cause a 50% increase in the twitch was about 3 times larger than needed to elicit the same response in vasa from rats treated with a placebo. The simultaneous administration of naloxone plus morphine partially antagonized tolerance development by about 22%. Morphine tolerance was extended to other opiate-like alkaloids such as etonitazene and a derivative of azidomorphine (CAM). In contrast to the effects of morphine, .beta.-endorphin inhibited neuromuscular transmission. Vasa from rats chronically treated with morphine were about 10 times less sensitive to the inhibitory effect of .beta.-endorphin as compared to paired placebo-treated controls. Chronic naloxone treatment in conjunction with morphine significantly reduced the cross-opiate tolerance by 66%. Morphine may interact at 2 different sites in the nerve terminals of the rat vas deferens.
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    EVIDENCE FOR MORPHINE AND MORPHINE-LIKE ALKALOID RESPONSES RESISTANT TO NALOXONE BLOCKADE IN THE RAT VAS-DEFERENS
    (1979) MIRANDA, H; HUIDOBRO, F; HUIDOBROTORO, JP
    The application of morphine or surrogates to the isolated rat was deferens maintained at 37.degree. C in Tyrode solution produced an increase in the electrically induced muscular twitch. Leucine enkephal in or D-2-D-Ala-Met enkephalinamide produced a dose-dependent inhibition of the muscular twitch. The effect of morphine and derivatives was not antagonized by naloxone, but the depression caused by the opiate pentapeptides or .beta.-endorphin was readily antagonized and reversed by naloxone. Tolerance developed to the in vitro effect of morphine; vasa deferentia obtained from tolerant-dependent rats were about 6 .times. less sensitive to the effect of morphine and about 5 .times. less sensitive to the depression caused by leucine enkephalin as compared to their respective paired, placebo implanted control rats.
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    INTERACTIONS BETWEEN MORPHINE AND THE OPIOID-LIKE PEPTIDES IN THE RAT VAS-DEFERENS
    (1980) HUIDOBRO, F; HUIDOBROTORO, JP; MIRANDA, H
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    NATURAL-RESISTANCE TO EFFECTS OF MORPHINE IN OCTODON-DEGUS A SOUTH-AMERICAN RODENT
    (1984) PAEILE, C; CONTRERAS, S; MIRANDA, H; VILLANUEVA, L; BUSTOS, E
    O. degus, a South American caviomorph, presents a natural resistance to some effects of morphine. None of the doses of morphine (i.v.) employed produced a significant modification of respiration rate. The administration of morphine leu-enkephalin and .beta.-endorphin to isolated O. degus vas deferens did not significantly change electrically-induced muscular twitches. Brain concentration of 14C morphine in the rat, as compared to O. degus, showed statistically significant differences. Pentazocine modified in EEG of O. degus, while morphine had no effect. Pimozide produced only a partial change of the pentazocine effect on EEG. This result is consistent with the view that pentazocine interacts with different opiate receptors.
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    NON-COMPETITIVE-NON-EQUILIBRIUM ALPHA-ADRENOCEPTOR BLOCKING PROPERTIES OF N-BENZYL IODOACETAMIDE, BETSAMIDE
    (1979) HUIDOBROTORO, JP; HUIDOBRO, F; MIRANDA, H
    N-Benzyl iodoacetamide, betsamide, at 10 mg/kg i.v. blocked the hypertensive and contractile responses of the nictitating membrane of the cat to adrenaline [epinephrine]. The blockade had a lag period before full development. Pretreatment of cats with betsamide for 7 or 18 h showed a non-equilibrium type of .alpha.-adrenoceptor blockade. The responses of the nictitating membrane to adrenaline were markedly depressed and did not recover after high doses of adrenaline. In the same cats, adrenaline caused a profound hypotension. The effect of betsamide lasted for at least 72 h. In the rat isolated vas deferens, 3 .times. 10-5 M betsamide non-competitively blocked the contractile responses to noradrenaline [norepinephrine], the adrenoceptor blockade was less effective when betsamide was applied with noradrenaline. The blockade lasted for > 24 h and was not reversible after extensive washing. Betsamide antagonized the contractile effects of the guinea pig trachea to adrenaline and isoprenaline. Results are discussed in relation to a probable mechanism of action.
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    VAS-DEFERENS DESENSITIZATION BY NORADRENALINE AND OTHER DRUGS
    (1976) MIRANDA, H
    Desensitization of the isolated rat vas deferens was demonstrated by using noradrenaline, 5-hydroxytryptamine, carbachol, acetylcholine or BaCl2 as a test concentration after a large concentration (concentration producing a contraction that was 80% of the maximum) of the same agonist. The large concentration of noradrenaline caused desensitization in response to 5-hydroxytryptamine and acetylcholine but not to carbachol and BaCl2. Desensitization is not altered by reserpine.sbd.in pretreatment of rats with reserpine or reserpine in Tyrode solution.sbd.imipramine and 6-hydroxydopamine. Surgical denervation or modification of the Na and Ca concentration of the Tyrode solution did not either alter desensitization. Results show that in the rat isolated vas deferens desensitization is not mediated by an action of noradrenaline on the adrenergic neuron.