RESUMO
The activity of receptor-operated Ca2+ channels (ROCCs) was studied in rat portal vein in L-thyroxine-induced experimental hyperthyroidism. The following parameters were evaluated: 1. NE-stimulated 45Ca influx. 2. CaCl2-induced contractile responses in Ca2+ free NE-stimulated tissues to calculate EC50 value of CaCl2. The NE (10(-6)mol) stimulated 45Ca influx and the mean EC50 value of CaCl2 did not differ significantly in portal veins isolated from hyperthyroid rats as compared to those of euthyroid control rats. The study revealed no significant change in the functional status of ROCCs in experimental hyperthyroidism.
Assuntos
Animais , Canais de Cálcio/metabolismo , Sinalização do Cálcio , Hipertireoidismo/induzido quimicamente , Masculino , Músculo Liso Vascular/metabolismo , Veia Porta/metabolismo , Ratos , Ratos Sprague-Dawley , Receptores Adrenérgicos alfa/metabolismo , Tiroxina/toxicidadeRESUMO
Effect of pinacidil, a K+ channel opener, was studied on contractility of cyclophosphamide-treated rat vas deferens. The mean IC50 value of pinacidil against 1 mmol barium chloride induced rhythmic contractions and 40 mmol potassium chloride induced tonic contractions was significantly (P < 0.01 and P < 0.001, respectively) increased in the cyclophosphamide treated group as compared to the control. The mean EC50 value of norepinephrine (NE) in the presence of pinacidil (10(-6) mol) was significantly (P < 0.001) increased in the cyclophosphamide treated group. These findings indicate that the responsiveness of rat vas deferens smooth muscle to pinacidil is reduced following cyclophosphamide treatment.
Assuntos
Animais , Antineoplásicos Alquilantes/toxicidade , Cálcio/metabolismo , Ciclofosfamida/toxicidade , Masculino , Norepinefrina/farmacologia , Pinacidil/farmacologia , Canais de Potássio/efeitos dos fármacos , Ratos , Ducto Deferente/efeitos dos fármacosRESUMO
Oestradiol acts both as a mitogen and as an inducer of differentiation of target cells. The cellular responses to oestradiol are generally mediated through the regulation of gene expression, although nongenomic modes of action are also documented. The present observations show that the regulation of keratin gene expression in rat vaginal epithelial cells is under the influence of oestradiol. It is observed that oestradiol regulates both the qualitative and quantitative expressions of keratin polypeptides in a time dependent and sequence specific manner. These regulatory effects are the result of modulations in transcriptional, post-transcriptional and translational processes of these genes, brought about by the hormone in vaginal epithelial cells.