Navegando por Palavras-chave "carbachol"
Agora exibindo 1 - 4 de 4
Resultados por página
Opções de Ordenação
- ItemSomente MetadadadosDifferent pathways for Ca2+ mobilization by angiotensin II and carbachol in the circular muscle of the guinea-pig ileum(Elsevier B.V., 1999-02-12) Shimuta, S. I.; Borges, ACR; Prioste, R. N.; Paiva, T. B.; Universidade Federal de São Paulo (UNIFESP)Ca2+ pathways activated by angiotensin II and carbachol were evaluated in the circular muscle of the guinea-pig ileum by recording mechanical and electrical activities. Transient contractions induced by angiotensin II were greatly reduced by Ca2+ removal from the medium whereas carbachol-induced responses were not significantly altered. Nifedipine had no effect on the responses to both agonists. A high concentration of tetrodotoxin (0.1 mu M) inhibited angiotensin II-induced contractile responses without affecting the depolarization, whereas 1 mM Ni2+ inhibited the mechanical and electrical effects. Neither tetrodotoxin nor Ni2+ affected carbachol-induced effects. These results indicate that angiotensin II-induced phasic contractions depend on extracellular Ca2+ but not on voltage-dependent L-type Ca2+ channels. It is suggested that angiotensin II activates Ni2+-sensitive Na+ and non-specific cationic channels, whereas the responses to carbachol are dependent on receptor-activated Ca2+ release. Furthermore the different response of the longitudinal and circular muscles to the inhibitory effects of tetrodotoxin and Ni2+ on the angiotensin II- and carbachol-induced contractions indicates that these agonists exert their own myogenic effects on each layer and are able to trigger different Ca2+ mobilization pathways. (C) 1999 Elsevier Science B.V. All rights reserved.
- ItemSomente MetadadadosEffect of estrogen on muscarinic acetylcholine receptor expression in rat myometrium(Elsevier B.V., 2004-01-15) Abdalla, FMF; Marostica, E.; Picarelli, Z. P.; Abreu, L. C.; Avellar, MCW; Porto, C. S.; Universidade Federal de São Paulo (UNIFESP); Inst ButantanWe report the effect of acute estrogen treatment in the expression of muscarinic acetylcholine receptors (mAChRs) in myometrium. Strips were obtained from rats in estrus (control) and treated with estrogen, 24 It before the experiments. Reverse transcriptase-polymerase chain reaction (RT-PCR) was performed and m2, m3 and m5 mAChR mRNA subtypes were detected in myometrium from both groups. [H-3]Quinuclidinyl benzilate ([(3)HQNB]) binding studies indicated that estrogen treatment did not change the affinity and density of mAChRs in myometrial membranes. Displacement curves of [(3)HQNB] with different mAChRs antagonists indicated a one-site fit for all antagonists tested. Comparison of pK(i) values indicated a significant correlation to M-2-mAChR subtype. Functional studies, however, showed that estrogen treatment increased myometrium sensitivity to carbachol and the calculated apparent affinity values were significantly correlated to M-3-mAChR. Furthermore, the pharmacological profile of the two populations of mAChR was not affected by estrogen. in conclusion, these results provide evidence for the presence of M-2- and M-3-mAChR, at the mRNA and protein level, in the rat myometrium and indicate that estrogen induces an increase in myometrial responsiveness to mAChR agonists. (C) 2003 Elsevier Ireland Ltd. All rights reserved.
- ItemSomente MetadadadosEffects of carbachol on rat Sertoli cell proliferation and muscarinic acetylcholine receptors regulation: an in vitro study(Elsevier B.V., 2004-08-20) Lucas, TFG; Avellar, MCW; Porto, C. S.; Universidade Federal de São Paulo (UNIFESP)The aim of the present work was to study the effect of muscarinic agonist on cell proliferation and muscarinic acetylcholine receptors (mAChRs) regulation in rat Sertoli cells. Primary cultures of Sertoli cells were obtained from 8-day and, 15-day old male Wistar rats. in proliferation assays, [methyl-H-3]thymidine incorporation in Sertoli cells from 8-day and 15-day old rats reached a plateau after 60 min of carbachol incubation and decreased after 120 min of agonist incubation. Binding studies with [N-Methyl-H-3]scopolamine ([H-3]NMS) indicated a rapid loss of cell surface mAChRs when Sertoli cells from 15-day old rats were incubated with carbachol at 35 degreesC for 2 min. This effect was temperature-dependent. When the incubation of the cells was prolonged at 35 degreesC or at 4 degreesC, after the agonist had been washed away, 94% of mAChRs were present in the cell surface after 120 min incubation at 35 degreesC. At 4 degreesC, however, a low percentage of mAChRs was detected in the cell surface. in the presence of cycloheximide, the recycling of mAChRs to the cell surface was not changed, suggesting that the appearance of mAChRs on cell surface was not dependent on de novo receptor synthesis. in conclusion, our studies indicate that the activation of mAChRs may play a role in rat Sertoli cell proliferation. These receptors may be under regulation (internalization and recycling) when cells are exposed to muscarinic cholinergic agonist. (C) 2004 Elsevier Inc. All rights reserved.
- ItemSomente MetadadadosIntracellular calcium mobilization by muscarinic receptors is regulated by micromolar concentrations of external Ca2+(Springer, 2001-06-01) Smaili, Soraya Soubhi [UNIFESP]; Carvalho, Solange Maria Torchia [UNIFESP]; Cavalcanti, Paulo MS [UNIFESP]; Jurkiewicz, Neide H. [UNIFESP]; Garcia, Antonio G.; Jurkiewicz, Aron [UNIFESP]; Universidade Federal de São Paulo (UNIFESP); Univ Autonoma MadridCarbachol-induced contractions of rat stomach fundus strips, obtained in a nutrient solution containing 1.8 mM Ca2+, were resistant to Ca2+ withdrawal, even after 1 h of bathing the tissues in a nominal 0 Ca2+ solution. This was not observed when K+ was used to evoke contractions, which were rapidly inhibited after Ca2+ removal (t(1/)2=2 min). the effect of carbachol in 0 Ca2+ solution was reduced by using drugs that reduce intracellular pools of Ca2+, such as caffeine (1-3 mM), ryanodine (30 muM) or thapsigargin (1 muM), corroborating the involvement of intracellular Ca2+ stores. On the other hand, when the 0 Ca2+ solution contained EGTA, a complete decline of carbachol effects was observed within about 8 min, indicating the involvement of extracellular Ca2+. Atomic absorption spectrometry showed that our 0 Ca2+ solution still contained 45 muM Ca2+, which was drastically reduced to 5.9 nM in the presence of EGTA. Taken together, our results indicate that the effects of carbachol are due to the mobilization of caffeine-, ryanodine- and thapsigargin-sensitive intracellular Ca2+ stores, and that these stores are not inactivated or depleted if micromolar concentrations (45 muM), but not nanomolar concentrations (5.9 nM) of Ca2+ are maintained in the extracellular milieu.