Abstract:Neurons which release atrial natriuretic peptide (ANPergic neurons) have their cell bodies in the paraventricular nucleus and in a region extending rostrally and ventrally to the anteroventral third ventricular (AV3V) region with axons which project to the median eminence and neural lobe of the pituitary gland. These neurons act to inhibit water and salt intake by blocking the action of angiotensin II. They also act, after their release into hypophyseal portal vessels, to inhibit stressinduced ACTH release, to… Show more
“…The same authors also demonstrated that ANG II receptorcontaining neurons of the SFO project to the DRN (Tanaka et al 1998), which suggests that this pathway monitors circulating ANG II levels mediated by volume and/or sodium depletion. In summary, based on the above observations and evidence provided by Lind (1986), Johnson & Thunhorst (1997), McCann et al (1997), Fitch & Weiss (2000) and Franchini et al (2002), afferent information is conveyed to the NTS and from there to the DRN and ANG II-sensitive forebrain areas through pressure and/or volume receptors and renal sensors of tubular sodium load. At another level, increased circulating ANG II concentrations, reflecting body fluid volume and/or sodium depletion and a later increase in salt intake, are detected by the SFO, which conveys information to the DRN for the modulation of current sodium appetite.…”
The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg kg _1 , I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food deprivation (deprived) by 31 and 45 %, respectively, 120 min after FEN injection, compared to HTR that received vehicle alone. Similarly, administration of FEN to ETR reduced 1.8 % NaCl intake in depleted and deprived rats by 64 and 46 %, respectively. The presynaptic serotonin reuptake inhibitor fluoxetine (20.0 mg kg _1 , I.P.) led to the inhibition of sodium appetite in HTR during the initial 30 min in depleted rats and for up to 60 min post-injection in deprived rats, while sodium appetite inhibition persisted for longer periods in ETR. The 5HT2C receptor agonist mCPP (5.0 mg kg _1 , I.P.) caused a drastic reduction in sodium appetite in HTR and ETR in depleted and deprived rats, respectively, after 120 min. Prior administration of the 5HT2C receptor antagonist LY53857 (5.0 mg kg _1 , I.P.) completely blocked the inhibitory action of mCPP on sodium appetite in both HTR and ETR. In summary, our results suggest that the recruitment of serotoninergic neurons involved in the modulation of sodium appetite seems to be decreased in hypothyroidism due to a probable deficiency in the cerebral signalling pathway.
“…The same authors also demonstrated that ANG II receptorcontaining neurons of the SFO project to the DRN (Tanaka et al 1998), which suggests that this pathway monitors circulating ANG II levels mediated by volume and/or sodium depletion. In summary, based on the above observations and evidence provided by Lind (1986), Johnson & Thunhorst (1997), McCann et al (1997), Fitch & Weiss (2000) and Franchini et al (2002), afferent information is conveyed to the NTS and from there to the DRN and ANG II-sensitive forebrain areas through pressure and/or volume receptors and renal sensors of tubular sodium load. At another level, increased circulating ANG II concentrations, reflecting body fluid volume and/or sodium depletion and a later increase in salt intake, are detected by the SFO, which conveys information to the DRN for the modulation of current sodium appetite.…”
The aim of the present work was to investigate the role of the serotoninergic system in the control of sodium appetite of hypothyroid rats (HTR) by administering drugs that affect the serotoninergic activity, and to compare the same homeostatic behaviour in euthyroid rats (ETR) also given these drugs. Fenfluramine (FEN; 5.0 mg kg _1 , I.P.), which releases serotonin in the brain, significantly reduced the intake of 1.8 % NaCl in HTR subjected to water and sodium depletion (depleted) or water, sodium and food deprivation (deprived) by 31 and 45 %, respectively, 120 min after FEN injection, compared to HTR that received vehicle alone. Similarly, administration of FEN to ETR reduced 1.8 % NaCl intake in depleted and deprived rats by 64 and 46 %, respectively. The presynaptic serotonin reuptake inhibitor fluoxetine (20.0 mg kg _1 , I.P.) led to the inhibition of sodium appetite in HTR during the initial 30 min in depleted rats and for up to 60 min post-injection in deprived rats, while sodium appetite inhibition persisted for longer periods in ETR. The 5HT2C receptor agonist mCPP (5.0 mg kg _1 , I.P.) caused a drastic reduction in sodium appetite in HTR and ETR in depleted and deprived rats, respectively, after 120 min. Prior administration of the 5HT2C receptor antagonist LY53857 (5.0 mg kg _1 , I.P.) completely blocked the inhibitory action of mCPP on sodium appetite in both HTR and ETR. In summary, our results suggest that the recruitment of serotoninergic neurons involved in the modulation of sodium appetite seems to be decreased in hypothyroidism due to a probable deficiency in the cerebral signalling pathway.
“…CNS cholinergic stimulation contributed to the natriuretic effect, indicating the involvement of brain cholinergic system. Similarly, injection of carbachol into lateral ventricle, septal area, and preoptic region exerted the natriuresis and diuresis (Colombari et al 1992;McCann et al 1997).…”
Abstract. The central nervous system is known to play important roles in the regulation of renal sodium excretion. The present study was designed to reveal the interrelationship between cholinergic pathway in the magnocellular paraventricular nucleus (PVN) and the natriuresis induced by brain cholinergic stimuli. The results indicated that urinary sodium excretion was significantly increased at 40 min after intracerebroventricular (ICV) injection of carbachol (CBC). Immunohistochemical studies showed that CBC increased choline acetyltransferase-immunoreactivity (ChAT-IR) in the magnocellular PVN and renal proximal convoluted tubule (PCT), respectively. After pretreatment with atropine, urinary sodium excretion was significantly reduced, and carbachol-increased ChAT-IR in the magnocellular PVN and PCT was also significantly decreased. These results suggested that brain cholinergic stimuli induced the natriuresis and increased the activity of cholinergic neurons in the magnocellular PVN and cholinergic system in the PCT. The blockade of muscarinic receptor completely abolished the natriuresis and partially inhibited carbachol-exerted stimulatory effects in the magnocellular PVN and PCT. To summarize, brain cholinergic pathway and peripheral cholinergic system in kidney were found to contribute to the natriuresis following brain cholinergic stimulation. Our findings revealed novel evidence that PVN was involved in the natriuresis via humoral mechanisms.
“…It has been shown that many brain-specific natriuretic factors are located in periventricular structures related to water and salt balance control (3)(4)(5), demonstrating a possible link between insulin and natriuresis. Alternatively, we also cannot rule out the possibility that central NO-dependent neural pathways may control cholinergic, adrenergic or non-adrenergic non-cholinergic neurons and/or the hypothalamic/pituitary release of hormones, which in turn acutely modulates the action of insulin in the brain.…”
Section: Discussionmentioning
confidence: 99%
“…This observation has led to speculation that insulin may play a role in the development of increased blood pressure (1,2). On the other hand, the role of the central nervous system (CNS) in the control of blood pressure and hydroelectrolyte homeostasis has been demonstrated by several studies (3)(4)(5). Further studies of insulin action on neurons have demonstrated pleiotropic effects on ion flows (6), neurotransmitter uptake and release (7), cell growth, survival, and the transcriptional regulation of genes involved with differentiation (8), as well as possible modulation of several brain functions, such as food intake regulation, reproductive function and cardiovascular function (2,(9)(10)(11).…”
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