Hipertensäo arterial / High blood pressure

Os autores inicialmente apresentam dados de consensos nacionais e internacionais sobre os valores normais da pressäo arterial, conceituando a hipertensäo arterial de acordo com os critérios atuais para o diagnóstico preciso da doença, considerando a distribuíçäo dos valores tensionais na populaçäo geral e as lesöes da hipertensäo arterial sobre os órgäos-alvo, bem como os fatores de risco cardiovascular associados. O tratamento näo farmacológico deve ser aplicado a todos os pacientes, com base na modificaçäo do estilo de vida a fim de reduzir ou eliminar os fatores de risco para a hipertensäo arterial e para as doenças cardiovasculares, incluindo a reduçäo do peso corporal, diminuíçäo da ingestäo de sódio, aumento da ingestäo de potássio, reduçäo de bebidas alcoólicas, realizaçäo de exercícios físicos, abandono do tabagismo, controle das dislipidemias e do diabetes e evitar o uso de drogas que possam aumentar a pressäo arterial. No tratamento farmacológico, os autores tecem comentários sobre a monoterapia e as associaçöes, apresentando o grupo de agentes utilizados: diuréticos, simpatolíticos (incluindo beta-bloqueadores), bloqueadores dos canais de cálcio, inibidores da enzima conversora da angiotensina, antagonistas dos receptores da angiotensina; mensionam os agentes de cada grupo, salientando as açöes farmacológicas, principais características, efeitos adversos, benefícios e detalhes sobre a utilizaçäo desses agentes na prática clínica.(au)

Astroglial and microglial reaction after a partial nigrostriatal degeneration induced by the striatal injection of different doses of 6-hydroxydopamine.

Astroglial and microglial activation was analyzed in adult male Wistar rats after a unilateral striatal injection of different doses (8, 4 and 1 micrograms) of 6-hydroxydopamine (6-OHDA). Control animals received the injection of the same volume of the solvent. The rotational behavior was registered by a rotometer 24 and 72 hours, 7, 10, 14 and 22 days after lesion. Following, animals were sacrificed and the tyrosine hydroxylase (TH) positive dopamine cells, the glial fibrillary acidic protein (GFAP) immunolabeled astrocytes and the OX42 immunoreactive microglia were visualized by mean of immunohistochemistry and quantified by stereologic method employing the optical disector and the point intercepts. The apomorphine (0.5 mg/kg)-induced circling behavior was seen only after 8 micrograms of 6-OHDA from 72 hours postlesion until sacrifice. Decreases of the TH immunoreactive terminals and cell bodies were found in the sampled fields of the striatum and pars compacta of the substantia nigra (SNc), respectively, after 8 and 4 micrograms of 6-OHDA. The GFAP immunohistochemistry revealed increases in the number/density of astroglial cells in the ipsilateral neostriatum (137% of control) and ipsilateral SNc (83% of control) and also in the volumeal fraction of the astroglial processes in the ipsilateral neostriatum (30% of control) and ipsilateral SNc (38% of control) in the rats with higher dose of the neurotoxin. Increases in the number of OX42 microglial labeled profiles and in the volumeal fraction of microglial processes were found in the ipsilateral neostriatum (67% and 27%, respectively, of control) and ipsilateral SNc (100% and 50%, respectively, of control) in the 8 micrograms 6-OHDA injected rats. These results suggest that the retrograde degeneration induced by a intrastriatal injection of a small dose of the 6-OHDA leads to an astroglial and microglial reaction in the nigrostriatal dopamine pathway. The interaction between activated glial cells may be involved in the wounding and repair events in the partial lesioned nigrostriatal system as well as in the paracrine responses to surviving dopamine neurons.

Muscarinic antagonists microinjected into the subthalamic nucleus decrease muscular rigidity in reserpinized rats.

The ability of anticholinergic agents microinjected into the subthalamic nucleus to reduce reserpine-induced muscular rigidity was assessed in rats. The electromyographical activity of the gastrocnemius-soleus muscle was used as a parameter of muscular rigidity. Reserpine (5 mg/kg i.p.) produced the appearance of electromyographical activity. The muscarinic antagonists M3 (1.27 nmol of 4-DAMP) and M1 (2.36 nmol of pirenzepine) markedly reduced the reserpine-induced electromyographical activity, whereas the M2 antagonist AFDX-116 (2.37 nmol) had no effect. These results suggest that a high cholinergic tone in the subthalamic nucleus is associated with the reserpine-induced muscular rigidity. Moreover, the M3 muscarinic antagonist is more effective than the M1 muscarinic antagonist in reducing the muscular rigidity in reserpinized rats, a model of Parkinson's disease, by blocking the high cholinergic tone in the subthalamic nucleus.