Adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion

Pillar, Alice X.; Silva-Netto, C. R.; Camargo, Laa; Saad, Wilson Abrão; Antunes‐Rodrigues, José; Covian, Miguel R.

doi:10.1016/0091-3057(77)90064-8

Cited by 23 publications

(11 citation statements)

References 17 publications

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“…The adrenergic pathways of the septal area in the regulation of electrolyte and water excretion demonstrated that the stimu lating and inhibitory effects are mediated by a-and (3-adrenoceptors, repectively [1]. Similar results were obtained with adren ergic stimulation of the lateral hypothalamic area [15], The ventromedial hypothalamus (VMH) shows a higher density of a-adrenergic sites than the lateral hypothalamic area [ 12].…”

Section: Introductionsupporting

confidence: 71%

Effects of the Application of α1and α2-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Saad¹,

Camargo²,

Saad³

1984

Pharmacology

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The effects of sodium and potassium excretion after intrahypothalamic administration of two α-adrenoceptor agonists and the effect of α-adrenoceptor antagonists were studied in groups of rats. Prazosin was equally effective at blocking the natriuretic and kaliuretic responses to the α₁-adrenoceptor agonist phenylephrine and the mixed α₁/α₂-adrenoceptor agonist noradrenaline, while yohimbine which acts preferentially on α₂-adrenoceptors was effective in potentiating these responses. These results suggest the presence of two types of α-adrenoceptors for the modulation of ventromedial hypothalamic pathways that interfere with the regulation of the two cations: stimulation of α₁-adrenoceptors facilitates, while stimulation of adrenoceptors inhibits the excretion of the ions.

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Section: Introductionsupporting

confidence: 71%

Effects of the Application of α1and α2-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Saad¹,

Camargo²,

Saad³

1984

Pharmacology

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“…jection of norepinephrine or hypertonic saline; these results suggest that a hormonal pathway mediates the effects ofthese stimuli on sodium excretion (7). Since we have shown that the cholinergic, adrenergic, or osmotic stimulation of tissue adjacent to the 3V induces natriuresis and kaliuresis (5)(6)(7)(8)(9)(10)(11) and since ANP is localized in these structures (19), in the present experiments, we determined if the effects on sodium excretion of stimulation and ablation of the AV3V region might be mediated, at least in part, by altered ANP release.…”

mentioning

confidence: 99%

“…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).…”

mentioning

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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“…Central injection of an α-adrenergic antagonist suppresses water intake induced by intracerebroventricular (icv) ANGII (6,7). Several areas of the limbic system participate in the regulation of sodium, potassium and water excretion (8). Previous studies have demonstrated the effects of α-antagonists and agonists injected into the lateral hypothalamus on the water and sodium intake induced by ANGII injection into the subfornical organ (3).…”

Section: Introductionmentioning

confidence: 99%

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

Saad

Guarda

Camargo

et al. 2002

Braz J Med Biol Res

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We investigated the role of α-adrenergic antagonists and clonidine injected into the medial septal area (MSA) on water intake and the decrease in Na + , K + and urine elicited by ANGII injection into the third ventricle (3rdV). Male Holtzman rats with stainless steel cannulas implanted into the 3rdV and MSA were used. ANGII (12 nmol/µl) increased water intake (12.5 ± 1.7 ml/120 min). Clonidine (20 nmol/ µl) injected into the MSA reduced the ANGII-induced water intake (2.9 ± 0.5 ml/120 min). Pretreatment with 80 nmol/µl yohimbine or prazosin into the MSA also reduced the ANGII-induced water intake (3.0 ± 0.4 and 3.1 ± 0.2 ml/120 min, respectively). Yohimbine + prazosin + clonidine injected into the MSA abolished the ANGIIinduced water intake (0.2 ± 0.1 and 0.2 ± 0.1 ml/120 min, respectively). ANGII reduced Na + (23 ± 7 µEq/120 min), K + (27 ± 3 µEq/120 min) and urine volume (4.3 ± 0.9 ml/120 min). Clonidine increased the parameters above. Clonidine injected into the MSA abolished the inhibitory effect of ANGII on urinary sodium. Yohimbine injected into the MSA also abolished the inhibitory effects of ANGII. Yohimbine + clonidine attenuated the inhibitory effects of ANGII. Prazosin injected into the MSA did not cause changes in ANGII responses. Prazosin + clonidine attenuated the inhibitory effects of ANGII. The results showed that MSA injections of α 1 -and α 2 -antagonists decreased ANGII-induced water intake, and abolished the Na + , K + and urine decrease induced by ANGII into the 3rdV. These findings suggest the involvement of septal α 1 -and α 2 -adrenergic receptors in water intake and electrolyte and urine excretion induced by central ANGII. Correspondence

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Adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion

Cited by 23 publications

References 17 publications

Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

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

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

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Adrenergic stimulation of the lateral hypothalamic area on sodium and potassium excretion

Cited by 23 publications

References 17 publications

Effects of the Application of &alpha;<sub>1</sub>and &alpha;<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Effects of the Application of &alpha;<sub>1</sub>and &alpha;<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

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

Adrenoceptors of the medial septal area modulate water intake and renal excretory function induced by central administration of angiotensin II

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Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion

Effects of the Application of α<sub>1</sub>and α<sub>2</sub>-Adrenoceptor Agonists and Antagonists into the Ventromedial Hypothalamus on the Sodium and Potassium Renal Excretion