MECANISMOS FISIOLÓGICOS E FISIOPATOLÓGICOS DETERMINANTES DA ATIVIDADE VASOMOTORA SIMPÁTICA

The sympathetic vasomotor activity is one of determinants of blood pressure (BP). Understanding the mechanisms involved in the control of the cardiovascular system is important in physiological and pathophysiological condition. The principal sympathetic premotor brain nuclei are confined in the paraventricular nucleus of hypothalamus (PVN) and in the rostralventrolateral medulla (RVLM). In different patophysiological condition, there is an increase in the sympathetic vasomotor tone, in part due to an increase in the activity of the PVN and RVLM neurons. In this brief review, we discussed the major mechanisms of sympathetic activation in different experimental models: 1) renovascular hypertension, 2) renoprival hypertension, 3) cardiac failure, 4) hypertension induced by nitric oxide blockade, 5) obesity and 6) gender differences. The actions of different mediators in the PVN and in the RVLM acting in long term, can change the level of sympathetic nerve activity and blood pressure and therefore, contributing for the progression of cardiovascular disease.A atividade vasomotora simpática é um dos determinantes da pressão arterial (PA). Estabelecer quais são os mecanismos geradores dessa atividade é importante para o entendimento de como o sistema cardiovascular opera, tanto em situações fisiológicas como fisiopatológicas. Os principais grupos pré-motores do simpático estão confinados no núcleo paraventricular do hipotálamo (PVN) e região rostoventrolateral bulbar (RVLM). Em diversas situações fisiopatológicas há aumento na atividade vasomotora simpática, em parte conseqüente a maior atividade dos neurônios do PVN e RVLM. Nesta breve revisão, foram discutidos os principais mecanismos de ativação simpática em diferentes modelos experimentais: 1) hipertensão renovascular, 2) hipertensão por baixa massa renal, 3) insuficiência cardíaca, 4) hipertensão por bloqueio do óxido nítrico, 5) obesidade e 6) dimorfismo sexual. As ações de diferentes mediadores sobre o PVN e RVLM podem em longo prazo determinar novos patamares de atividade simpática, modificando os níveis tensionais e dessa forma, contribuir para a progressão da doença cardiovascular

NEURAL MECHANISMS INVOLVED in the RECOVERY FROM INSULIN HYPOGLYCEMIA in DOGS

NIMH,CEREBRAL METAB LAB,BETHESDA,MD 20205UNIV São Paulo,INST BIOMED SCI,DEPT PHYSIOL & PHARMACOL,BR-05508 São Paulo,SP,BRAZILEscola Paulista de MedicinaWeb of Scienc

TIME COURSE of INSULIN, CORTICOSTERONE and METABOLIC CHANGES CAUSED BY LESION of the VENTROMEDIAL HYPOTHALAMUS in the RAT

ESCOLA PAULISTA MED,DEPT PHYSIOL,DIV NEUROPHYSIOL & ENDOCRINE PHYSIOL,BR-04023 São Paulo,SP,BRAZILESCOLA PAULISTA MED,DEPT PHYSIOL,DIV NEUROPHYSIOL & ENDOCRINE PHYSIOL,BR-04023 São Paulo,SP,BRAZILWeb of Scienc

Effects of continuous exposure to light on behavioral dopaminergic supersensitivity

Background: This study examines the effects of long-term continuous exposure to light on dopaminergic supersensitivity induced by repented treatment with haloperidol in rats,Methods: Spontaneous general activity in an open-field (SGA) and stereotyped behavior induced by apomorphine (SB-APO) or amphetamine (SB-AMP) were used as experimental parameters. Rats were allocated to four groups in each experiment: saline-treated animals kept under a 12-hour light/dark cycle (LD) or 24-hour light/light cycle (LL), and 2 mg/kg haloperidol-treated animals kept under the above cycles. Plasma corticosterone concentration was also measured by radioimunoassay in saline-treated mts kept under a LD or LL cycle.Results: All the behavioral parameters used showed the development of central dopaminergic supersensitivity in rats kept under both cycles. Continuous exposure to light enhanced SGA and SB-AMP in both saline- and haloperidol-treated mts, but did not modify SB-APO. Animals kept under the LL cycle presented an increased plasma corticosterone concentration.Conclusions: Our results suggest that continuous exposure to light leads to an increase in dopaminergic function in both normal and supersensitive rats. This effect seems to be mediated by a presynaptic mechanism possibly involving corticosterone actions. (C) 1999 Society of Biological Psychiatry.Universidade Federal de São Paulo, Escola Paulista Med, Dept Farmacol, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Fisiol, BR-04023062 São Paulo, BrazilUniv São Paulo, Inst Biociencias, Dept Fisiol, São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Farmacol, BR-04023062 São Paulo, BrazilUniversidade Federal de São Paulo, Escola Paulista Med, Dept Fisiol, BR-04023062 São Paulo, BrazilWeb of Scienc

Effect of chemical stimulation of the dorsomedial hypothalamic nucleus on blood plasma glucose, triglycerides and free fatty acids in rats

The effects of chemical stimulation of the dorsomedial hypothalamic nucleus (DMH) on blood plasma concentration of glucose, triglycerides, insulin, and free fatty acids (FFA) were investigated in anesthetized adult Wistar rats. Microinjection of 12.5 nmol of norepinephrine into the DMH increased blood plasma concentration of glucose and FFA, decreased triglycerides, and did not change plasma insulin within 5 min; after 20 min, blood glucose and FFA reached control values. Microinjection of epinephrine (12.5 nmol) into the DMH also increased blood plasma glucose concentration and decreased triglycerides after 5 min. These effects are probably mediated by beta-adrenergic mechanisms, because they were prevented by beta-adrenergic antagonist propranolol, but not by alpha-adrenergic antagonist prazosin. Microinjection into the DMH of glutamate, dopamine, or acetylcholine failed to cause any change in those metabolic parameters, corroborating the hypothesis that the DMH is part of a beta-adrenergic pathway involved in short-term modulation of the availability of glucose and FFA. Copyright (C) 1997 Elsevier Science Inc.UNIV ESTADUAL LONDRINA,DEPT QUIM,BR-86051 LONDRINA,PR,BRAZILUNIV ESTADUAL CAMPINAS,DEPT PHYSIOL,BR-13081970 CAMPINAS,SP,BRAZILUniversidade Federal de São Paulo,DEPT FISIOL,São Paulo,BRAZILUNIV São Paulo,FAC MED,BR-05508 São Paulo,BRAZILUniversidade Federal de São Paulo,DEPT FISIOL,São Paulo,BRAZILWeb of Scienc

NEONATAL TREATMENT WITH MONOSODIUM GLUTAMATE INCREASES PLASMA-CORTICOSTERONE in the RAT

ESCOLA PAULISTA MED,DEPT MED,DIV ENDOCRINOL,BR-04023 São Paulo,SP,BRAZILESCOLA PAULISTA MED,DEPT MORPHOL,DIV HISTOL,BR-04023 São Paulo,SP,BRAZILESCOLA PAULISTA MED,DEPT MED,DIV ENDOCRINOL,BR-04023 São Paulo,SP,BRAZILESCOLA PAULISTA MED,DEPT MORPHOL,DIV HISTOL,BR-04023 São Paulo,SP,BRAZILWeb of Scienc