11 research outputs found
Phosphoinositide hydrolysis mediated by H1 receptors in autoimmune myocarditis mice
Stimulation of phosphoinositide hydrolysis in myocardium from autoimmune myocarditis mice by ThEA and histamine was assayed. Myocardium from autoimmune heart, but not the normal forms, specifically increased phosphoinositide turnover in the presence of histaminergic agonists. This increment was blocked by a specific H1 antagonist mepyramine and to the same extent by the phospholipase C inhibitor NCDC. By using a binding assay H1 histaminergic receptors were detected in autoimmune heart membrane preparations, but this was not observed in normal heart. These data suggest that autoimmune myocardium expressed a functional H1 receptor that could involve a distinctive mechanism operating in the disease
Cholinoceptor Activation Subserving the Effects of Interferon Gamma on the Contractility of Rat Ileum
Recombinant rat interferon Îł stimulated the contractility of
isolated rat ileum at doses of 4–12 units/ml. Muscarinic
cholinoceptors were involved, as treatment of the tissue with
atropine prevented the contractile response of the ileum.
Furthermore, interferon Îł increased the affinity of carbachol for
the cholinoceptors and did not change its maximum effect. Neurogenic
pathways were also involved since pretreatment of ileum with
hexamethonium, hemicholinium or tetrodotoxin impaired the
contractile effect of interferon Îł. In contrast to the action of
exogenous carbachol, the effects of interferon Îł are indirect. They
appear to involve a G protein regulating phosphoinositide turnover
and cytoskeletal structures since they could not be induced in ileum
strips that were pretreated with pertussis toxin, phospholipase C
inhibitors (2-nitro-carboxyphenyl, NN-diphenyl carbamate and
neomycin), cytochalasine B or colchicine
Increase nitric oxide synthase activity in parotid glands from rats with experimental periodontitis
OBJECTIVE: In this study we investigated the activity of the nitric oxide synthase (NOS) in parotid glands from rats with experimental periodontitis and controls. METHODS: Periodontitis was produced by a ligature placed around the cervix of the two lower first molar. Experiments were carried out 22 days after the ligature. RESULTS: Ligation caused an increase in parotid NOS activity. The selective blocker of the inducible isoform of the enzyme partially inhibited its activity in parotid glands from rat with ligature. In controls, the activity was partially inhibited by the antagonists of the selective neural and endothelial isoforms. NOS activity in rats with ligature was cyclic adenosine monophosphate (cAMP)-dependent while in controls it was calcium-dependent. Prostaglandin Eâ‚‚ concentration was increased in parotid gland from rats with ligature. The inhibitor of prostaglandin production, FR 122047, diminished both, prostaglandin production and NOS activity. In rats with ligature unstimulated amylase released is increased. Both, prostaglandin and NOS were involved in the increment of amylase release. CONCLUSION: It can be concluded that in parotid glands from ligated rats, prostaglandin Eâ‚‚ production is increased and, through cAMP accumulation, activates the inducible NOS isoform. The increment of nitric oxide production participates in the increase in basal amylase release.Fil: Miozza, V.. Universidad de Buenos Aires. Facultad de OdontologĂa. Cátedra de FarmacologĂa; ArgentinaFil: Borda, Enri Santiago. Consejo Nacional de Investigaciones CientĂficas y TĂ©cnicas; Argentina. Universidad de Buenos Aires. Facultad de OdontologĂa. Cátedra de FarmacologĂa; ArgentinaFil: S-Borda, L.. Universidad de Buenos Aires. Facultad de OdontologĂa. Cátedra de FarmacologĂa; ArgentinaFil: Busch, L.. Universidad de Buenos Aires. Facultad de OdontologĂa. Cátedra de FarmacologĂa; Argentin