Identification of pathways involved in the natriuretic, kaliuretic and diuretic responses induced by cholinergic stimulation of the medial septal area (MSA)

Franci, Celso Rodrigues; Antunes‐Rodrigues, José; Silva-Netto, C. R.; Camargo, Laa; Saad, Wilson Abrão

doi:10.1016/0031-9384(83)90039-2

Cited by 11 publications

(6 citation statements)

References 41 publications

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“…Other evidence indicates that, besides the AV3V, other structures such as the MnPO, SFO, medial septal area, anterior lateral hypothalamus, SON, PVN, medial habenula, and stria medullaris are organized into a neural circuit involved in the regulation of water/sodium intake and excretion (90,170,172,432). Neurons in the PVN, MnPO, preoptic and hypothalamic periventricular nuclei, median eminence, and OVLT also contain ␣-ANP as determined by immunocytochemistry (245,267,268,363,401,573), which suggests that ANP neurons may be one of the effectors involved in control of water and salt intake.…”

Section: B Osmotic Control Of Vasopressin Releasementioning

confidence: 99%

“…Thus it became clear that both ␣-adrenergic and cholinergic synapses are involved in the control of both natriuresis and kaliuresis. Microinjection of agonists and antagonists of these neurotransmitters into the septal area, AV3V, or the third ventricle altered the natriuretic, kaliuretic, and carbachol-induced antidiuretic responses (72,73,120,170,172,351,365,431,432,443,444). Phentolamine, an ␣-adrenergic antagonist, abolished the natriuretic response to third ventricle injection of hypertonic saline, norepinephrine, or carbachol.…”

Section: Introductionmentioning

confidence: 98%

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Neuroendocrine Control of Body Fluid Metabolism

Antunes‐Rodrigues

Castro

Elias

et al. 2004

Physiological Reviews

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Mammals control the volume and osmolality of their body fluids from stimuli that arise from both the intracellular and extracellular fluid compartments. These stimuli are sensed by two kinds of receptors: osmoreceptor-Na+ receptors and volume or pressure receptors. This information is conveyed to specific areas of the central nervous system responsible for an integrated response, which depends on the integrity of the anteroventral region of the third ventricle, e.g., organum vasculosum of the lamina terminalis, median preoptic nucleus, and subfornical organ. The hypothalamo-neurohypophysial system plays a fundamental role in the maintenance of body fluid homeostasis by secreting vasopressin and oxytocin in response to osmotic and nonosmotic stimuli. Since the discovery of the atrial natriuretic peptide (ANP), a large number of publications have demonstrated that this peptide provides a potent defense mechanism against volume overload in mammals, including humans. ANP is mostly localized in the heart, but ANP and its receptor are also found in hypothalamic and brain stem areas involved in body fluid volume and blood pressure regulation. Blood volume expansion acts not only directly on the heart, by stretch of atrial myocytes to increase the release of ANP, but also on the brain ANPergic neurons through afferent inputs from baroreceptors. Angiotensin II also plays an important role in the regulation of body fluids, being a potent inducer of thirst and, in general, antagonizes the actions of ANP. This review emphasizes the role played by brain ANP and its interaction with neurohypophysial hormones in the control of body fluid homeostasis.

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Section: B Osmotic Control Of Vasopressin Releasementioning

confidence: 99%

Section: Introductionmentioning

confidence: 98%

Neuroendocrine Control of Body Fluid Metabolism

Antunes‐Rodrigues

Castro

Elias

et al. 2004

Physiological Reviews

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397

310

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“…The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1)(2)(3)(4)(5)(6)(7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1)(2)(3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4).…”

Section: Central Nervous System and Hydromineral Balancementioning

confidence: 99%

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Ventura

Gomes

Reis

et al. 2002

Braz J Med Biol Res

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The central nervous system plays an important role in the control of renal sodium excretion. We present here a brief review of physiologic regulation of hydromineral balance and discuss recent results from our laboratory that focus on the participation of nitrergic, vasopressinergic, and oxytocinergic systems in the regulation of water and sodium excretion under different salt intake and hypertonic blood volume expansion (BVE) conditions. High sodium intake induced a significant increase in nitric oxide synthase (NOS) activity in the medial basal hypothalamus and neural lobe, while a low sodium diet decreased NOS activity in the neural lobe, suggesting that central NOS is involved in the control of sodium balance. An increase in plasma concentrations in vasopressin (AVP), oxytocin (OT), atrial natriuretic peptide (ANP), and nitrate after hypertonic BVE was also demonstrated. The central inhibition of NOS by L-NAME caused a decrease in plasma AVP and no change in plasma OT or ANP levels after BVE. These data indicate that the increase in AVP release after hypertonic BVE depends on nitric oxide production. In contrast, the pattern of OT secretion was similar to that of ANP secretion, supporting the view that OT is a neuromodulator of ANP secretion during hypertonic BVE. Thus, neurohypophyseal hormones and ANP are secreted under hypertonic BVE in order to correct the changes induced in blood volume and osmolality, and the secretion of AVP in this particular situation depends on NOS activity. Central nervous system and hydromineral balancePrecise regulation of body fluid osmolality is essential. Osmolality is controlled by a finely tuned, intricate homeostatic mechanism that operates by adjusting both the rate of water intake and excretion. The central nervous system (CNS) plays an important role in the control of renal sodium excretion (1-7). Considerable evidence indicates that the median preoptic area (MnPO), anterior lateral hypothalamus, subfornical organ (SFO), anterior portion of the third ventricle (AV3V), supraoptic nucleus (SON), paraventricular nucleus (PVN), organum vasculosum laminae terminalis (OVLT), habenula, stria medullaris, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (1-3). Natriuresis accompanied by kaliuresis is induced by cholinergic or adrenergic stimulation of the medial septal area, MnPO, anterior lateral hypothalamus, SFO, and AV3V (1,4). Stimulation of AV3V with carbachol, a cholinergic drug, angiotensin II or hypertonic saline enhances natriuresis, which is blocked by the destruction of this brain area (1,4-7). Neurohypophyseal hormones and the control of sodium and water excretionAlthough the neuroendocrine control of sodium and water balance is not completely understood, alterations in volume and osmolality are responsible, at least in part, for changes in plasma vasopressin (AVP) concentration. Verney (8) originally demonstrated that AVP release into the blood is stimulated by the activation of os...

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“…Cholinergic or adrenergic stimulation of the medial septal area, medial preoptic area, anterior lateral hypothalamus, and subfornical organ as well as the anterior portion of the third ventricle (AV3V) induces a dose-related natriuresis accompanied by a lesser kaliuresis (5)(6)(7)(8)(9)(10)(11)(12)(13)(14)(15)(16)(17). Thus, considerable evidence indicates that the medial preoptic area, anterior lateral hypothalamus, subfornical organ, AV3V, habenula, stria medullaris, supraoptic nucleus, and medial septal area are organized in a neural circuit involved in the regulation of water and sodium intake and excretion (12,13,17). The AV3V plays a key role in central control of sodium excretion since its stimulation by carbachol (5-17), a cholinergic drug, angiotensin II (All) or hypertonic saline (18) enhances and its destruction blocks sodium excretion in goats (18) and rats (15,16).…”

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confidence: 99%

Role of the hypothalamus in the control of atrial natriuretic peptide release.

Baldissera

Menani

Santos

et al. 1989

Proc. Natl. Acad. Sci. U.S.A.

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Stimulation of the region antero-ventral to the third cerebral ventricle (AV3V) by a cholinergic drug, carbachol, and lesions of the AV3V have been demonstrated in previous studies to either augment or decrease sodium excretion, respectively. Atrial natriuretic peptide (ANP) dramatically increases renal sodium excretion and has been localized to brain areas previously shown to be involved in control of sodium excretion. Consequently, to evaluate a possible role of brain ANP in evoking the changes in renal sodium excretion that follow stimulations or lesions of the AV3V, we determined the effect of injection of carbachol into the AV3V of rats on the concentration of plasma ANP and its content in several neural tissues, the pituitary gland, lungs, and atria. Conversely, the effect of lesions in the AV3V on plasma ANP and the content of the polypeptide in the various organs was determined. Injection of carbachol into the AV3V produced the expected natriuresis, which was accompanied within 20 min by a dramatic rise in the plasma ANP concentration and a rise in ANP content in the medial basal hypothalamus, the neurohypophysis, and particularly the anterior hypophysis but without alterations in the content of ANP in the lungs or the right or left atrium. Conversely, there was a dramatic decline in plasma ANP at both 24 and 120 hr after the AV3V lesions had been placed. This was accompanied by a slight decline in the content of the peptide in the lungs. There was no change in its content in the right atrium at 24 hr after lesions, but there was a significant increase at 120 hr. There was a small decline in the content in the left atrium at 24 hr, followed by a rebound to slightly elevated levels at 120 hr. These small changes contrasted sharply with the dramatic decline in content of the peptide in the medial basal hypothalamus, median eminence, neurohypophysis, choroid plexus, anterior hypophysis, and olfactory bulb. These declines persisted or became greater at 120 hr; except in the olfactory bulb in which the decline was no longer significant. The dramatic increase in plasma ANP after carbachol stimulation of the AV3V that was accompanied by marked elevations in content of the peptide in basal hypothalamus and neuro-and adenohypophysis suggests that the natriuresis resulting from this stimulation is brought about at least in part by release of ANP from the brain. Conversely, the dramatic decline in plasma ANP after AV3V lesions was accompanied by very dramatic declines in content of ANP in these same structures, which suggests that the previously shown decrease in sodium excretion obtained after these lesions may be at least in part due to a decrease in release of ANP from the brain. In view of the much larger quantities of the peptide stored in the atria, it is still possible that changes in atrial release may contribute to the alterations in plasma ANP observed after stimulation or ablation of the AV3V region; however, these results suggest that the dramatic changes in plasma ANP that followed these manipu...

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Identification of pathways involved in the natriuretic, kaliuretic and diuretic responses induced by cholinergic stimulation of the medial septal area (MSA)

Cited by 11 publications

References 41 publications

Neuroendocrine Control of Body Fluid Metabolism

Neuroendocrine Control of Body Fluid Metabolism

Nitrergic modulation of vasopressin, oxytocin and atrial natriuretic peptide secretion in response to sodium intake and hypertonic blood volume expansion

Role of the hypothalamus in the control of atrial natriuretic peptide release.

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