Moxonidine and central α2 adrenergic receptors in sodium intake

Oliveira, Lisandra Brandino de; Luca, Laurival A. De; Menani, José Vanderlei

doi:10.1016/j.brainres.2003.09.011

Cited by 10 publications

(11 citation statements)

References 21 publications

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Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

“…Peripheral administration of clonidine and moxonidine also inhibits water and sodium intake, whereas peripheral administration of yohimbine has the opposite effect (40,57,93,132). Central antagonism of ␣ 2 -adrenoceptors by yohimbine or RX 821002 reduces the antinatriorexigenic effects of lipopolysaccharide, which suggests that central adrenergic mechanisms are involved in the inhibition of sodium intake in pathological conditions such as bacterial or viral infections (1).…”

Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

“…The effects of ␣ 2 -adrenoceptor or ␣ 2 -adreno/imidazoline receptor agonists on sodium and water intake are reversed by the pretreatment with ␣ 2 -adrenoceptor antagonists (e.g., yohimbine, RX 821002, or SK&F86466), which suggests that the activation of ␣ 2 -adrenoceptors plays a role in the inhibition of water and sodium intake (40,47,93,125). The increased efficacy provided by the imidazoline moiety to several ␣ 2 -adrenoceptor agonists and antagonists suggests a synergic action between imidazoline receptors and ␣ 2 -adrenoceptors acting to inhibit water and salt intake (40,93,125).Peripheral administration of clonidine and moxonidine also inhibits water and sodium intake, whereas peripheral administration of yohimbine has the opposite effect (40,57,93,132). Central antagonism of ␣ 2 -adrenoceptors by yohimbine or RX 821002 reduces the antinatriorexigenic effects of lipopolysaccharide, which suggests that central adrenergic mechanisms are involved in the inhibition of sodium intake in pathological conditions such as bacterial or viral infections (1).…”

mentioning

confidence: 99%

“…In contrast, blood volume expansion releases humoral factors, such as atrial natriuretic peptide (ANP), which inhibit salt and water intake (5,6,14,49). Other agonists and receptor subtypes, such as oxytocin and ␣ 2 -adrenoceptors, act in the brain to inhibit behavioral responses that expand body fluids (12,13,39,40,48,93,123,125).ANG II and hyperosmolarity act on sites that function as sensory structures, specifically the OVLT, SFO, and AP, which are located outside the blood-brain barrier. In some cases they also act on structures located within the blood-brain barrier such as the supraoptic nucleus of the hypothalamus (25, 26, 75-77, 84, 86, 118, 119).…”

mentioning

confidence: 99%

“…Similar to norepinephrine, either intracerebroventricular or forebrain parenchimal injections into the lateral hypothalamus, medial septal area, or preoptic area of ␣ 2-adrenoceptor agonists (e.g., ␣-methylnorepinephrine) or of ␣ 2 -adrenergic-imidazoline receptor agonists (e.g., clonidine or moxonidine) also inhibit water and sodium intake (39,40,47,93,125). The effects of ␣ 2 -adrenoceptor or ␣ 2 -adreno/imidazoline receptor agonists on sodium and water intake are reversed by the pretreatment with ␣ 2 -adrenoceptor antagonists (e.g., yohimbine, RX 821002, or SK&F86466), which suggests that the activation of ␣ 2 -adrenoceptors plays a role in the inhibition of water and sodium intake (40,47,93,125). The increased efficacy provided by the imidazoline moiety to several ␣ 2 -adrenoceptor agonists and antagonists suggests a synergic action between imidazoline receptors and ␣ 2 -adrenoceptors acting to inhibit water and salt intake (40,93,125).…”

mentioning

confidence: 99%

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Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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.-In states of sodium deficiency many animals seek and consume salty solutions to restore body fluid homeostasis. These behaviors reflect the presence of sodium appetite that is a manifestation of a pattern of central nervous system (CNS) activity with facilitatory and inhibitory components that are affected by several neurohumoral factors. The primary focus of this review is on one structure in this central system, the lateral parabrachial nucleus (LPBN). However, before turning to a more detailed discussion of the LPBN, a brief overview of body fluid balance-related body-to-brain signaling and the identification of the primary CNS structures and humoral factors involved in the control of sodium appetite is necessary. Angiotensin II, mineralocorticoids, and extracellular osmotic changes act on forebrain areas to facilitate sodium appetite and thirst. In the hindbrain, the LPBN functions as a key integrative node with an ascending output that exerts inhibitory influences on forebrain regions. A nonspecific or general deactivation of LPBN-associated inhibition by GABA or opioid agonists produces NaCl intake in euhydrated rats without any other treatment. Selective LPBN manipulation of other neurotransmitter systems [e.g., serotonin, cholecystokinin (CCK), corticotrophin-releasing factor (CRF), glutamate, ATP, or norepinephrine] greatly enhances NaCl intake when accompanied by additional treatments that induce either thirst or sodium appetite. The LPBN interacts with key forebrain areas that include the subfornical organ and central amygdala to determine sodium intake. To summarize, a model of LPBN inhibitory actions on forebrain facilitatory components for the control of sodium appetite is presented in this review. sodium intake; angiotensin; electrolyte balance; thirst ANIMALS CONSTANTLY LOSE WATER and electrolytes to the external environment, but specific autonomic, hormonal, and behavioral mechanisms operate continuously to adjust and restore body fluid-electrolyte balance. The rate of loss from the kidneys is primarily controlled by neural and hormonal actions, but loss may also occur passively through the largely uncontrolled processes of respiration (evaporation), perspiration, transpiration, and salivation. These later modes of loss are referred to as insensible loss because they cannot be easily measured. Severe loss of both sodium and water may also occur in disorders associated with emesis and diarrhea. However, despite such ongoing challenges, the osmolarity and volume of body fluids are maintained within reasonably narrow limits, thus allowing normal metabolic and cardiovascular functions. Although renal mechanisms can slow water and sodium loss, the restoration of fluid homeostasis is only made possible by the mobilization of behaviors that result in the ingestion of water and sodium (usually NaCl). The behavioral responses of seeking out and consuming water and salty substances involve the motivational states of thirst and salt appetite. Salt appetite is also frequently referred to as sodium appetit...

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Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

Section: Major Neurohumoral Factors Inhibiting Water And/or Sodium Inmentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

mentioning

confidence: 99%

See 3 more Smart Citations

Role of the lateral parabrachial nucleus in the control of sodium appetite

Menani

Luca

Johnson

2014

American Journal of Physiology-Regulatory, Integrative and Comp

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Involvement of central α1- and α2-adrenoceptors on cardiovascular responses to moxonidine

Moreira

Takakura

Menani

et al. 2007

European Journal of Pharmacology

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Involvement of central α1-adrenoceptors on renal responses to central moxonidine and α-methylnoradrenaline

Andrade

Paula

et al. 2009

European Journal of Pharmacology

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Moxonidine (alpha2-adrenoceptor/imidazoline receptor agonist) injected into the lateral ventricle induces diuresis, natriuresis and renal vasodilation. Moxonidine-induced diuresis and natriuresis depend on central imidazoline receptors, while central alpha1-adrenoceptors are involved in renal vasodilation. However, the involvement of central alpha1-adrenoceptors on diuresis and natriuresis to central moxonidine was not investigated yet. In the present study, the effects of moxonidine, alpha-methylnoradrenaline (alpha2-adrenoceptor agonist) or phenylephrine (alpha1-adrenoceptor agonist) alone or combined with previous injections of prazosin (alpha1-adrenoceptor antagonist), yohimbine or RX 821002 (alpha2-adrenoceptor antagonists) intracerebroventricularly (i.c.v.) on urinary sodium, potassium and volume were investigated. Male Holtzman rats (n = 5-18/group) with stainless steel cannula implanted into the lateral ventricle and submitted to gastric water load (10% of body weight) were used. Injections of moxonidine (20 nmol) or alpha-methylnoradrenaline (80 nmol) i.c.v. induced natriuresis (196 +/- 25 and 171 +/- 30, respectively, vs. vehicle: 101 +/- 9 microEq/2 h) and diuresis (9.0 +/- 0.4 and 12.3 +/- 1.6, respectively, vs. vehicle: 5.2 +/- 0.5 ml/2 h). Pre-treatment with prazosin (320 nmol) i.c.v. abolished the natriuresis (23 +/- 4 and 76 +/- 11 microEq/2 h, respectively) and diuresis (5 +/- 1 and 7.6 +/- 0.8 ml/2 h, respectively) produced by i.c.v. moxonidine or alpha-methylnoradrenaline. RX 821002 (320 nmol) i.c.v. abolished the natriuretic effect of alpha-methylnoradrenaline, however, yohimbine (320 nmol) did not change renal responses to moxonidine. Phenylephrine (80 nmol) i.c.v. induced natriuresis and kaliuresis that were blocked by prazosin. Therefore, the present data suggest that moxonidine and alpha-methylnoradrenaline acting on central imidazoline receptors and alpha2-adrenoceptors, respectively, activate central alpha1-adrenergic mechanisms to increase renal excretion.

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Moxonidine and central α2 adrenergic receptors in sodium intake

Cited by 10 publications

References 21 publications

Role of the lateral parabrachial nucleus in the control of sodium appetite

Role of the lateral parabrachial nucleus in the control of sodium appetite

Involvement of central α1- and α2-adrenoceptors on cardiovascular responses to moxonidine

Involvement of central α1-adrenoceptors on renal responses to central moxonidine and α-methylnoradrenaline

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