IMPORTÂNCIA DA REGIÃO ANTEROVENTRAL DO TERCEIRO VENTRÍCULO (AV3V) NO CONTROLE CARDIOVASCULAR E DO EQUILÍBRIO HIDROELETROLÍTICO

A manutenção da pressão arterial em níveis normais é importante para a homeostasia do meio interno. O sistema nervoso central regulando a atividade dos eferentes autonômicos simpático e parassimpático ajusta a pressão arterial possibilitando ao animal ou ao ser humano um melhor desempenho frente a diferentes situações do cotidiano. Diferentes áreas centrais são responsáveis pelo controle das descargas autonômicas sobre o sistema cardiovascular e muitas delas também participam do controle do equilíbrio hidroeletrolítico. Uma dessas áreas é o tecido periventricular ao redor da porção anteroventral do terceiro ventrículo (região AV3V) localizado no prosencéfalo e que é uma das principais áreas centrais onde se localizam receptores da angiotensina II e osmorreceptores. A lesão da região AV3V impede o desenvolvimento de diversas formas de hipertensão experimental em ratos e dificulta o aparecimento de respostas pressoras produzidas por diversos estímulos. A lesão da região AV3V também reduz respostas dipsogênicas induzidas pela angiotensina II, estimulação colinérgica central, privação hídrica e aumento de osmolaridade plasmática, a secreção do peptídeo natriurético atrial produzida pela expansão de volume e a excreção renal de sódio produzida pela estimulação colinérgica central. Evidências mais recentes também sugerem uma participação da região AV3V nas respostas pressoras produzidas pela ativação de mecanismos bulbares.The maintenance of the arterial pressure in normal levels is important for the homeostasis of body fluids. The central nervous system regulating sympathetic and parasympathetic autonomic efferent can adjust arterial pressure which allows animals or human to face different daily activities with the best performance. Different central areas are responsible for the control of autonomic discharges to cardiovascular system and many of them are also involved in the control of fluid electrolyte balance. One of these areas is the tissue surrounding the anteroventral third ventricle (AV3V region) localized in the forebrain and a main central site for angiotensin II receptors and osmoreceptors. The AV3V lesions impair the development of many models of experimental hypertension in rats and the pressor responses to different stimuli. Lesions of the AV3V region also reduce dipsogenic responses to angiotensin II, central cholinergic activation, water deprivation and increase in plasma osmolarity, atrial natriuretic peptide secretion produced by body fluid expansion and the increase in renal excretion to central cholinergic activation. Recent evidence also suggests the participation of AV3V region in pressor responses produced by the  activation of medullary mechanisms

IMPORTÂNCIA DA REGIÃO ANTEROVENTRAL DO TERCEIRO VENTRÍCULO (AV3V) NO CONTROLE CARDIOVASCULAR E DO EQUILÍBRIO HIDROELETROLÍTICO

The maintenance of the arterial pressure in normal levels is important for the homeostasis of body fluids. The central nervous system regulating sympathetic and parasympathetic autonomic efferent can adjust arterial pressure which allows animals or human to face different daily activities with the best performance. Different central areas are responsible for the control of autonomic discharges to cardiovascular system and many of them are also involved in the control of fluid electrolyte balance. One of these areas is the tissue surrounding the anteroventral third ventricle (AV3V region) localized in the forebrain and a main central site for angiotensin II receptors and osmoreceptors. The AV3V lesions impair the development of many models of experimental hypertension in rats and the pressor responses to different stimuli. Lesions of the AV3V region also reduce dipsogenic responses to angiotensin II, central cholinergic activation, water deprivation and increase in plasma osmolarity, atrial natriuretic peptide secretion produced by body fluid expansion and the increase in renal excretion to central cholinergic activation. Recent evidence also suggests the participation of AV3V region in pressor responses produced by the  activation of medullary mechanisms.A manutenção da pressão arterial em níveis normais é importante para a homeostasia do meio interno. O sistema nervoso central regulando a atividade dos eferentes autonômicos simpático e parassimpático ajusta a pressão arterial possibilitando ao animal ou ao ser humano um melhor desempenho frente a diferentes situações do cotidiano. Diferentes áreas centrais são responsáveis pelo controle das descargas autonômicas sobre o sistema cardiovascular e muitas delas também participam do controle do equilíbrio hidroeletrolítico. Uma dessas áreas é o tecido periventricular ao redor da porção anteroventral do terceiro ventrículo (região AV3V) localizado no prosencéfalo e que é uma das principais áreas centrais onde se localizam receptores da angiotensina II e osmorreceptores. A lesão da região AV3V impede o desenvolvimento de diversas formas de hipertensão experimental em ratos e dificulta o aparecimento de respostas pressoras produzidas por diversos estímulos. A lesão da região AV3V também reduz respostas dipsogênicas induzidas pela angiotensina II, estimulação colinérgica central, privação hídrica e aumento de osmolaridade plasmática, a secreção do peptídeo natriurético atrial produzida pela expansão de volume e a excreção renal de sódio produzida pela estimulação colinérgica central. Evidências mais recentes também sugerem uma participação da região AV3V nas respostas pressoras produzidas pela ativação de mecanismos bulbares

Enhancement of meal-associated hypertonic NaCl intake by moxonidine into the lateral parabrachial nucleus

α2-Adrenoceptor activation with moxonidine (α2-adrenergic/imidazoline receptor agonist) into the lateral parabrachial nucleus (LPBN) enhances angiotensin II/hypovolaemia-induced sodium intake and drives cell dehydrated rats to ingest hypertonic sodium solution besides water. Angiotensin II and osmotic signals are suggested to stimulate meal-induced water intake. Therefore, in the present study we investigated the effects of bilateral injections of moxonidine into the LPBN on food deprivation-induced food intake and on meal-associated water and 0.3 M NaCl intake. Male Holtzman rats with cannulas implanted bilaterally into the LPBN were submitted to 14 or 24 h of food deprivation with water and 0.3 M NaCl available (n = 6-14). Bilateral injections of moxonidine (0.5 nmol/0.2 μl) into the LPBN increased meal-associated 0.3 M NaCl intake (11.4 ± 3.0 ml/120 min versus vehicle: 2.2 ± 0.9 ml/120 min), without changing food intake (11.1 ± 1.2 g/120 min versus vehicle: 11.2 ± 0.9 g/120 min) or water intake (10.2 ± 1.5 ml/120 min versus vehicle: 10.4 ± 1.2 ml/120 min) by 24 h food deprived rats. When no food was available during the test, moxonidine (0.5 nmol) into the LPBN of 24 h food-deprived rats produced no change in 0.3 M NaCl intake (1.0 ± 0.6 ml/120 min versus vehicle: 1.8 ± 1.1 ml/120 min), nor in water intake (0.2 ± 0.1 ml/120 min versus vehicle: 0.6 ± 0.3 ml/120 min). The results suggest that signals generated during a meal, like dehydration, for example, not hunger, induce hypertonic NaCl intake when moxonidine is acting in the LPBN. Thus, activation of LPBN inhibitory mechanisms seems necessary to restrain sodium intake during a meal. © 2007 Elsevier B.V. All rights reserved

Inhibitory mechanism of the nucleus of the solitary tract involved in the control of cardiovascular, dipsogenic, hormonal, and renal responses to hyperosmolality

The nucleus of the solitary tract (NTS) is the primary site of visceral afferents to the central nervous system. In the present study, we investigated the effects of lesions in the commissural portion of the NTS (commNTS) on the activity of vasopressinergic neurons in the hypothalamic paraventricular (PVN) and supraoptic (SON) nuclei, plasma vasopressin, arterial pressure, water intake, and sodium excretion in rats with plasma hyperosmolality produced by intragastric 2 M NaCl (2 ml/rat). Male Holtzman rats with 15-20 days of sham or electrolytic lesion (1 mA; 10 s) of the commNTS were used. CommNTS lesions enhanced a 2 M NaCl intragastrically induced increase in the number of vasopressinergic neurons expressing c-Fos in the PVN (28 ± 1, vs. sham: 22 ± 2 c-Fos/AVP cells) and SON (26 ± 4, vs. sham: 11 ± 1 c-Fos/AVP cells), plasma vasopressin levels (21 ± 8, vs. sham: 6.6 ± 1.3 pg/ml), pressor responses (25 ± 7 mmHg, vs. sham: 7 ± 2 mmHg), water intake (17.5 ± 0.8, vs. sham: 11.2 ± 1.8 ml/2 h), and natriuresis (4.9 ± 0.8, vs. sham: 1.4 ± 0.3 meq/1 h). The pretreatment with vasopressin antagonist abolished the pressor response to intragastric 2 M NaCl in commNTS-lesioned rats (8 ± 2.4 mmHg at 10 min), suggesting that this response is dependent on vasopressin secretion. The results suggest that inhibitory mechanisms dependent on commNTS act to limit or counterbalance behavioral, hormonal, cardiovascular, and renal responses to an acute increase in plasma osmolality. © 2013 the American Physiological Society

Sodium intake combining cholinergic activation and noradrenaline into the lateral parabrachial nucleus

The administration of cholinergic agonists like pilocarpine intraperitoneally (i.p.) or carbachol intracerebroventricularly (i.c.v.) induces water, but non significant hypertonic NaCl intake. These treatments also produce pressor responses, which may inhibit sodium intake. Noradrenaline (NOR) acting on a2-adrenoceptors in the lateral parabrachial nucleus (LPBN) deactivates inhibitory mechanisms increasing fluid depletion-induced sodium intake. In the present study, we investigated: (1) water and 1.8% NaCl intake in rats treated with pilocarpine i.p. or carbachol i.c.v. combined with NOR into the LPBN; (2) if inhibitory signals from cardiovascular receptors are blocked by NOR in the LPBN. Male Holtzman rats with stainless steel guide-cannulas implanted in the lateral ventricle and bilaterally in the LPBN were used. Bilateral injections of NOR (80 nmol/0.2 ll) into the LPBN decreased water intake (0.8 ± 0.3, vs. saline (SAL): 2.9 ± 0.3 ml/180 min) induced by pilocarpine (1 mg/kg of body weight) i.p., without changing 1.8% NaCl intake (0.8 ± 2.4, vs. SAL: 0.5 ± 0.3 m l/180 min). Prazosin (1 mg/kg of body weight) i.p. blocked pressor responses and increased water and 1.8% NaCl intake (6.3 ± 1.7 and 14.7 ± 3.5 ml/180 min, respectively) in rats treated with pilocarpine combined with NOR into the LPBN. Prazosin i.p. also increased 1.8% NaCl intake in rats treated with carbachol i.c.v combined with NOR into the LPBN. The results suggest that different signals inhibit sodium intake in rats treated with cholinergic agonists, among them those produced by increases of arterial pressure that are not efficiently deactivated by NOR acting in the LPBNFundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)