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Biomedical subjects

J Roquebert

Publications and source records attributed to J Roquebert.

At least 55 records · Page 3Linked to original sources
PubMedDate not supplied

NPFF, a FMRF-NH2-like peptide, blocks opiate effects on ileum contractions.

We studied the ability of NPFF, a FMRFamide-like peptide with certain antiopiate properties, to affect the inhibitory effect of morphine on the electrically induced contraction of guinea pig ileum. Neuropeptide FF had no effect when administered alone but reduced morphine inhibition in a noncompetitive manner. Neuropeptide FF also altered the inhibitory effect of opioid peptides as released by an intense electrical stimulation at 10 Hz. These results suggest that NPFF receptors exist in guinea pig ileum in association with opiate receptors, and that endogenous NPFF may play a role in the diarrhea observed in the morphine withdrawal syndrome.

Animals↗
PubMedDate not supplied

[Differential inhibition of raubasine and tetrahydroalstonine on the vasopressor response to sympathetic nervous stimulation and intravenous noradrenaline in the pithed rat].

The effects of raubasine and tetrahydroalstonine (THA) on the vasopressor response to sympathetic nerve stimulation and to i.v. administration of noradrenaline were studied in the pithed rat to ascertain whether raubasine and THA would preferentially block pressor responses due to exogenous versus endogenous noradrenaline alpha-adrenergic receptor activation. Raubasine (0.5 to 4 mg/kg i.v.) was more effective in blocking the response due to sympathetic nerve stimulation than that due to i.v. noradrenaline. On the other hand THA (0.5 to 4 mg/kg i.v.) produced greater inhibition of the i.v. noradrenaline response than the sympathetic nerve stimulation response. THA (0.5, 1, 2 mg/kg i.v.) enhanced the nerve stimulation response, while at the 4 mg/kg dose the response was slightly reduced. This may be explained by a preferential block by THA at low doses, of presynaptic alpha 2-adrenoceptors. In pithed rat raubasine and THA showed dose-related blocking effects on the pressor response of phenylephrine and B-HT 933, respectively. This suggest that raubasine preferentially blocks alpha-1 and THA alpha 2-adrenoceptors. The results suggest that raubasine and THA preferentially block the pressor responses of post-synaptic alpha-adrenergic receptor activation due to endogenous and exogenous noradrenaline, respectively.

Adrenergic alpha-Agonists↗
PubMedDate not supplied

[Comparative study of the pre and post-synaptic alpha blocking activity of thymoxamine and its metabolites in the rat vas deferens (author's transl)].

1. The action of thymoxamine and its two metabolites at pre- and post-synaptic alpha-adrenoceptors have been studied on rat vas deferent. 2. Low frequency electrical stimulation of the rat isolated vas deferens produced regular contractions that were inhibited by low concentrations of clonidine. The inhibition of the vas deferens produced by clonidine was presynaptic in origin and involved alpha-adrenoceptors. 3. Presynaptic alpha-adrenoceptor antagonist activity was assessed by studying the effect of increasing concentrations of the antagonists on cumulative clonidine dose-response curves on the stimulated vas deferens. 4. Postsynaptic alpha-adrenoceptor antagonist activity was assessed by comparison of control cumulative noradrenaline dose-response curves with those in the presence of increasing concentrations of antagonists in the isolated vas deferens. 5. The results indicate that thymoxamine and its metabolites block postsynaptic alpha-adrenoceptors preferentially. Phentolamine is more potent in blocking presynaptic than postsynaptic alpha-adrenoreceptors. 6. At postsynaptic alpha-adrenoceptors thymoxamine and deacetylthymoxamine present nearly the same blocking activity, N-demethyl déacétylthymoxamine is less active. At presynaptic alpha-adrenoceptors their activity is practically negligible. 7. The findings support the view that pre- and post-synaptic alpha-adrenoceptors in the rat vas deferens differ in their sensitivity to alpha adrenoceptor antagonists.

Adrenergic alpha-Antagonists↗
PubMedDate not supplied

[Antinoradrenergic activity of raubasine on isolated thoracic aorta and vas deferens of rat (author's transl)].

1. The type and intensity of antagonism exerted by yohimbine and raubasine on the noradrenaline action have been studied in vitro. 2. Cumulative dose-response curves with noradrenaline as the agonist, were made using isolated thoracic aorta and vas deferens of rat kept in a Krebs solution. When an antagonist shift the curve to the right the competitive nature of the interaction was verified by assessing the regression straight line of log (x-I) on log (antagonist concentration) and calculation of pA2. 3. In rat isolated vas deferens, the isotonic contractile response to low doses of noradrenaline were antagonized and those to high does potentiated by raubasine. The alpha-adrenoceptor blocker thus caused a shift to the right and an increase of the maximum height of log dose-response curves of alpha-adrenoceptor stimulant. Yohimbine shift the dose-response curves to the right without change of maximal contraction. The curves were analysed with the Schhild plot, and the slopes obtained 0.82 (Yohimbine), 0.96 (Raubasine) were not significantly different from I. The pA2 value is of 6.10 for yohimbine and of 6.50 for raubasine. In the presence of cocaine, which blocks the neuronal uptake, the dose-response curves were shifted to the right in parallel without alteration of maximal contraction. The pA2 value is of 6.57 for yohimbine and of 6.75 for raubasine. Yohimbine and raubasine carry on a competitive type antagonism on the noradrenaline effect. 4. On the thoracic aorta, yohimbine (pA2 = 6.83) and raubasine (pA2 = 7.21) act as competitive antagonists.

Adrenergic alpha-Antagonists↗