Functional relationship between subfornical organ cholinergic stimulation and nitrergic activation influencing cardiovascular and body fluid homeostasis.

We have studied the effects of L-NG-nitro arginine methyl esther (L-NAME), L-arginine (LAR), inhibitor and a donating nitric oxide agent on the alterations of salivary flow, water intake, arterial blood pressure (MAP) and heart rate (HR) induced by the injection pilocarpine into the subfornical organ (SFO). Rats (Holtzman 250-300 g) were anesthetized with 2, 2, 2-tribromoethanol (20 mg/100 kg b. wt.) and a stainless steel cannula were implanted into their SFO. The volume of injection was 0.2 microl. The amount of saliva secretion was studied over a 5-min period. Pilocarpine (40 microg), L-NAME (40 microg) and LAR (30 microg) were used in all experiments for the injection into the SFO. Pilocarpine (10, 20, 40, 80 and 160 microg) injected into SFO elicited a concentration-dependent increase in salivary secretion. L-NAME injected prior to pilocarpine into the SFO increased salivary secretion and water intake due to the effect of pilocarpine. LAR injected prior to pilocarpine into the SFO attenuated the salivary secretion and water intake. Pilocarpine, injected into the SFO increased the MAP and decreased heart rate (HR). L-NAME injected prior to pilocarpine into the SFO potentiated the pressor effect of pilocarpine with a decrease in HR. LAR injected into the SFO prior to pilocarpine attenuated the increase in MAP with no changes in HR. The present study suggests that the SFO nitrergic cells interfere in the cholinergic pathways implicated in the control of salivary secretion, fluid and cardiovascular homeostasis.

Nitric oxide of the supraoptic nucleus influences the salivary secretion, sodium renal excretion, urinary volume and arterial blood pressure induced by pilocarpine.

Male Holtzman rats weighting 200-250 g were anesthetized with zoletil 50 mg/Kg (tiletamine chloridrate 125.0 mg and zolazepan chloridrate 125.0 mg) into quadriceps muscle and stainless steel cannulas were implanted into their supraoptic nucleus (SON). We investigated the effects of the injection into the supraoptic nucleus (SON) of FK 409, a nitric oxide donor, and NW-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase inhibitor (NOS), on the salivary secretion, arterial blood pressure, sodium excretion and urinary volume induced by pilocarpine, which was injected into SON. The drugs were injected in 0.5 microl volume over 30-60 s. Controls was injected with a similar volume of 0.15 M NaCl. FK 409 and L-NAME were injected at doses of 20 microg/0.5 microl and 40 microg/0.5 microl respectively. The amount of saliva secretion was studied over a five-minute period after injection of pilocarpine into SON. Injection of pilocarpine (10, 20, 40, 80, 160 microg/microl) into SON produced a dose-dependent increase in salivary secretion. L-NAME was injected into SON prior to the injection of pilocarpine into SON, producing an increase in salivary secretion due to the effect of pilocarpine. FK 409 injected into SON attenuating the increase in salivary secretion induced by pilocarpine. Mean arterial pressure (MAP) increase after injections of pilocarpine into the SON. L-NAME injected into the SON prior to injection of pilocarpine into SON increased the MAP. FK 409 injected into the SON prior to pilocarpine attenuated the effect of pilocarpine on MAP. Pilocarpine (0.5 micromol/0.5 microl) injected into the SON induced an increase in sodium and urinary excretion. L-NAME injected prior to pilocarpine into the SON increased the urinary sodium excretion and urinary volume induced by pilocarpine. FK 409 injected prior to pilocarpine into the SON decreased the sodium excretion and urinary volume induced by pilocarpine. All these roles of pilocarpine depend on the release of nitric oxide into the SON. In summary the present results show: a) SON is involved in pilocarpine-induced salivation; b) that mechanism involves increase in MAP, sodium excretion and urinary volume.

Role of nitric oxide and beta-adrenoceptors of the central nervous system on the salivary flow induced by pilocarpine injection into the lateral ventricle.

Our studies have focused on the effect of L-NG-nitroarginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), and L-arginine, the substrate of NOS, on salivary secretion induced by the administration of pilocarpine into the lateral cerebral ventricle (LV) of rats. The present study has also investigated the role of the beta-adrenergic agonists and antagonist injected into LV on the salivary secretion elicited by the injection of pilocarpine into LV. Male Holtzman rats with a stainless-steel cannula implanted into the LV were used. The amount of salivary secretion was studied over a 7-min period after injection of pilocarpine, isoproterenol, propranolol, salbutamol, salmeterol, L-NAME and L-arginine. The injection of pilocarpine (10, 20, 40, 80 and 160 microg/microl) into LV produced a dose-dependent increase in salivary secretion. The injection of L-NAME (40 microg/microl) into LV alone produced an increase in salivary secretion. The injection of L-NAME into LV previous to the injection of pilocarpine produced an increase in salivary secretion. L-Arginine (30 microg/microl) injected alone into LV produced no change in salivary secretion. L-Arginine injected into LV attenuated pilocarpine-induced salivary secretion. The isoproterenol (40 nmol/microl) injected into LV increased the salivary secretion. When injected previous to pilocarpine at a dose of 20 and 40 microg/microl, isoproterenol produced an additive effect on pilocarpine-induced salivary secretion. The 40-nmol/microl dose of propranolol injected alone or previous to pilocarpine into LV attenuated the pilocarpine-induced salivary secretion. The injection of salbutamol (40 nmol/microl), a specific beta-2 agonist, injected alone into LV produced no change in salivary secretion and when injected previous to pilocarpine produced an increase in salivary secretion. The 40-nmol/microl dose of salmeterol, a long-acting beta-2 agonist, injected into LV alone or previous to pilocarpine produced no change in salivary secretion. The results have shown that central injections of L-NAME and L-arginine interfere with the salivary secretion, which implies that might participate in pilocarpine-induced salivary secretion. The interaction between cholinergic and beta-adrenergic receptors of the central nervous system (CNS) for the control of salivary secretion can also be postulated.

Homeostase e organizaçäo: relaçäo entre os conceitos e introduçäo do tempo / Homeostasis and organization: relationship between concepts and introduction of time

Este artigo, de caráter introdutório, discute e revê algumas idéias a respeito do conceito de homeostase. Fatos e modelos temporais säo introduzidos para mostrar que existem mudanças de estado nos biossistemas que näo säo preditas pela homeostase. Conceitos de termodinâmica e de organizaçäo säo apresentados, fornecendo novas bases para se entender o estado de um biossistema

Influência dos adrenoceptores alfa1 e alfa2 do hipotálamo médio sobre a pressao arterial sistêmica em ratos / Role of the alfa1 and alfa2 adrenoceptores in the medial hypothalamus on the arterial pressure in rats

Foram estudados os efeitos sobre a pressäo arterial sistêmica após a administraçäo de noradrenalina e de dois antagonistas de alfa-adrenoceptores no hipotálamo médio de ratos normotensos. Tanto o prazosin quanto a ioimbina antagonizaram a açäo do agonista misto de alfa1/alfa2-adrenoceptores, a noradrenalina ; entretanto a administraçäo prévia de prazosin mostrou uma maior interaçäo da noradrenalina pelos adrenoceptores alfa1. Estes resultados sugerem que os adrenoceptores alfa1 do hipotálamo médio exerceriam uma maior influência que os adrenoceptores alfa2 no controle de pressäo arterial sistêmica

Effects of intracerebroventricular infusion of angiotensin II and related peptides on water and sodium ingestion and excretion

The objetive of the present study was to investigate the effects of an angiotensin II (AII) analogue, Des-Asp1-AII and of two competitive blockers, [Leu8]-AII and [octanoyl-Leu8]-AII, infused intracerebroventriculary on the ingestion of water and of a 3% NaCl solution, as well as on diuresis and natriuresis in normal rats and in adrenalectomized and deoxycorticosterone (DOCA)-treated rats. Both AII and Des-Asp1-AII increased water and 3% NaCl intake and increased urine and Na+ excretion, the effect of AII being more intense. Except for 3% NaCl, the responses of all other parameters were totally or partially reduced by previous treatment with [Leu8]-AII or [octanoyl-Leu8]-AII. Subcytaneous DOCA injection caused water ingestion. Previous treatment with DOCA increased the response to AII for the ingestion of 3% NaCl and inhibited sodium excretion. The results obtained for adrenalectomized rats treated with DOCA, AII and analogous agonists did not differ from those observed in normal rats. These data suggest a possible synergism between the cerebral and renal renin-angiotensin systems in the regulation of the physiological parameters studied

Papel dos adrenoceptores alfa1 e alfa2 do hipotálamo médio sobre a excreçäo de sódio e potássio / Role of alpha1 e alpha2 adrenoceptors of the medial hypothalamus on sodium and potassium excretion

Injeçäo de noradrenalina dentro do hipotálamo médio de ratos produziu uma estimulaçäo da excreçäo urinária de sódio e potássio. Ioimbina (10**-9 e 4.10**-9 M), um bloqueador dos adrenoceptores alfa 2, potencializou a excreçäo dos dois cátions quando injetado antes do agonista enquanto que o prazosin, um antagonista dos adrenoceptores alfa 1, inibiu estas respostas quando injetado nas mesmas doses. Por outro lado, injeçöes de clonidina, um agonista dos adrenoceptores alfa 2, dentro da mesma área produziu uma inibiçäo dose-dependente da excreçäo de Na+ e K+. O prazosin potencializou os efeitos da clonidina enquanto que a ioimbina inibiu estas repostas. Estes resultados sugerem a presença de dois tipos de adrenoceptores alfa para a modulaçäo das vias centrais que interferem com a regulaçäo dos dois cátions: a estimulaçäo dos adrenoceptores alfa 1 facilita enquanto a estimulaçäo dos adrenoceptores alfa 2 inibem a excreçäo dos ions

Effects of lesions in some areas of the central nervous system on serum concentrations of glucose, triglycerides, cholesterol, HDL-cholesterol and total lipids

Neste experimento estudamos, através de lesöes eletrolíticas em ratos, a participaçäo do complexo amigdalóide, área preóptica lateral, hipotálamo posterior, área septal e núcleo ventromediano, nos níveis circulantes de glicose, triglicerídeos, colesterol, lipídeos totais e HDL-colesterol. A lesäo no complexo amigdalóide näo determinou nenhuma alteraçäo significativa em nenhum dos componentes estudados, embora apresentasse tendência a aumento ou diminuiçäo de um ou outro componente. A lesäo da área preóptica lateral provocou queda significante nos níveis de triglicerídeos e aumento do HDL-colesterol. A lesäo do hipotálamo posterior provocou queda significante nos níveis de triglicerídeos, colesterol e lipídeos totais. A lesäo da área septal determinou aumento significante nos níveis de lipídeos totais. A lesäo do núcleo ventromediano determinou aumento significativo do HDL-colesterol. Estes resultados sugerem a participaçäo destas áreas do sistema nervoso central na regulaçäo do metabolismo lipídico

Efeito da aplicaçäo intracerebroventricular da angiotensina II e da des-amino-angiotensina II sobre a ingestäo de água, pressäo arterial e frequência cardíaca / Effect of intracerebroventricular infusion of angiotensin II and des-amino-angiotensin II on water intake , arterial pressure and heart rate

Os efeitos centrais da aplicaçäo no ventrículo cerebral lateral da angiotensina II (AII) e da des-amino-AII (des-NH2-AII) sobre a ingestäo de água, pressäo arterial e frequência cardíaca foram determinados em ratos. Os resultados demonstraram que tanto a AII como a des-NH2-AII exercem efeitos pressor e dipsogênico por açäo no sistema nervoso central. A des-NH2-AII näo influenciou na frequência cardíaca, embora seu efeito pressor tenha sido semelhante ao da AII. Pelos resultados obtidos podemos sugerir que os dois agonistas atuam no mesmo sistema de receptores, mas a des-NH2-AII apresenta afinidade e atividade ligeiramente maiores do que a AII