Cell-enlargement-related polypeptides are induced via beta(1)-adrenoceptors in mouse parotids.

Induction of cell and gland enlargement (growth-in-size) and induction of a group of secretory polypeptides (polypeptides C-G) seem to occur in close relationship in mouse parotid glands stimulated chronically by the nonselective beta-adrenergic agonist isoproterenol. To determine whether beta(1), beta(2), or both subtypes of beta-adrenergic receptors are involved in those responses, dose-dependency studies were carried out during a 7-day period of daily stimulations to assess the relative abilities of the selective beta-adrenergic agonists dobutamine (beta(1)) and salbutamol (beta(2)) to induce polypeptides C-G and growth-in-size. The relative abilities of the selective beta-adrenoceptor antagonists atenolol (beta(1)) and I.C.I. 118.551 (beta(2)) to interfere with the induction of both responses by chronic treatment with the various beta-adrenergic agonists were also studied. Parotid growth-in-size was assessed by evaluating wet weight, whole protein content, and light microscopy histology. The presence of polypeptides C-G was evaluated after SDS-polyacrylamide gel electrophoresis and Coomassie blue staining. Under these experimental conditions, dobutamine was found to be at least one order of magnitude more potent than salbutamol at inducing growth-in-size. Dobutamine was also found to be clearly stronger than salbutamol as an inducer of polypeptides C-G. On the other hand, atenolol was more effective than I.C.I. 118.551 at preventing the induction of polypeptides C-G and growth-in-size by isoproterenol, dobutamine, or salbutamol. Taken together, these results suggest that in mouse parotid glands, polypeptides C-G and growth-in-size are induced preferentially via adrenergic receptors of the beta(1)-subtype.

Transcriptional and posttranscriptional control in synthesis of growth marker polypeptides in mouse parotids.

The chronic daily administration of isoproterenol provokes in mouse parotid glands the induction and progressive accumulation of a family of secretory polypeptides named polypeptides C, D, E, F, and G (polypeptides C-G). These polypeptides, which seem to be part of the family of proline-rich proteins, have been considered as molecular markers of the growth-in-size response in the mouse parotid acinar cells. In the present study, two pharmacological approaches were used to determine whether the induction and the postsecretory reappearance of polypeptides C-G may be distinguished from each other. First, actinomycin D, a transcriptional inhibitor, was found to interfere with the induction by isoproterenol but not with the postsecretory reappearance. Second, pilocarpine, a secretagogue that was found to be a very weak inducer of polypeptides C-G, was able to provoke secretion and then reappearance of the whole group of isoproterenol-induced polypeptides. Accordingly, these data suggest that the induction of polypeptides C-G is dependent on transcriptional activity and that it is unrelated to secretion stimulation. By contrast, the postsecretory reappearance of polypeptides C-G may occur even when transcriptional activity is inhibited and it would be related to the secretory activity.

Consideraciones psicopatologicas en torno al uso de beta-bloqueadores en los sindromes angustiosos. / Psychopathological considerations on the use of beta-blockers in anyiety syndrome

Se revisan las indicaciones terapeuticas de los beta-bloqueadores en los sindromes angustiosos, concluyendo que solo son efectivos en los casos que se asocian a un claro sindrome vegetativo beta-adrenergico Se postula la existencia de dos tipos basicos de angustia (angustia de riesgo y angustia de responsabilidad), de diferente semiologia vegetativa y vinculados, respectivamente, al polo neurotico el efecto del propranolol sobre los componentes psiquicos y somaticos de la angustia y se postula que ambas experiencia estan igualmente vinculadas a la respuesta vegetativa y son susceptibles de correcion mediante bloqueo beta-adrenergico.Se discute el mecanismo central o periferico del efecto ansiolitico de los beta-bloqueadores y se senala que este puede ser explicado, en la mayoria de los casos, exclusivamente por el bloqueo de la retroalimentacion aferente sobre el sistema nervioso central

Modelo diagnostico del sintoma fobico neurotico. / Diagnosis model of the neurotic phobic symptom

Se critica el concepto clasico de neurosis fobica y se propone un modelo diagnostico del sintoma fobico neurotico basado principalmente en las observaciones clinicas y experimentales de la reflexologia y del aprendizaje.Este modelo constituye un concepto nosologico mas amplio que permite postular, junto al diagnostico tradicional de neurosis fobica, la existencia de mecanismos fobicos en diferentes sintomas neuroticos y psicosomaticos