Effects of catecholamines injected into the septal area of the rat brain on natriuresis, kaliuresis and diuresis

Camargo, Laa; Saad, Wilson Abrão; Netto, Cincinato Rodrigues Silva; Gentil, C; Antunes‐Rodrigues, José; Covian, Miguel R.

doi:10.1139/y76-034

Cited by 40 publications

(24 citation statements)

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“…The adrenergic pathways of the septal area play an important role in the regulation of electrolyte and water excretion. α-Adrenoceptors present an excitatory effect, whereas ß-adrenoceptors present an inhibitory effect (9,10). Rats with electrolytic lesions of the septal area drink more water than normal ones in response to thirst stimuli mediated by ANGII (11).…”

Section: Introductionmentioning

confidence: 99%

“…The natriuretic-kaliuretic response elicited by cholinergic stimulation of the lateral hypothalamic area depends in part on synapses located in the medial septal area (MSA), the response elicited by cholinergic stimulation of the MSA also utilizes synapses located in the lateral hypothalamic area (21). Increased renal sodium and potassium excretion has been obtained with noradrenaline and other adrenergic drugs injected into the septal area (9). There is some evidence that fibers from the subfornical organ converge to the nucleus medianus and also project to the supraoptic nucleus, paraventricular nucleus and throughout the lateral preoptic area-lateral hypothalamic area (22).…”

Section: Introductionmentioning

confidence: 99%

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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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Section: Introductionmentioning

confidence: 99%

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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“…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.…”

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confidence: 96%

“…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).…”

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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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“…The potential contributions of the central nervous system and kidneys in these models of chronic stress hypertension are suggested by studies of acute environmental stress. Acute exposure to air jet stress leads to antinatriuresis and an increase in renal sympathetic nerve activity that is much greater in nephrine into the ventromedial hypothalamus, lateral hypothalamus, septal area, or 3rd cerebral ventricle of conscious rats; this natriuresis is prevented by ai-adrenoceptor antagonists and is potentiated by a 2 -adrenoceptor antagonists (Camargo et al, 1976;Morris et al, 1977;Pillar et al, 1977;Saad et al, 1984). In contrast, an antinatriuresis follows the injection of isoproterenol into the lateral hypothalamus, septal area, or 3rd cerebral ventricle; this antinatriuresis is abolished by ft, 2 -or ft-, but not ft-adrenoceptor antagonists (Morris et al, 1977;Pillar et al, 1977;Camargo et al, 1979).…”

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confidence: 99%

Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats.

Koepke¹,

Jones²,

DiBona³

1986

Circulation Research

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SUMMARY. The contributions of /Si-, B^-, and a 2 -adrenoceptors in the posterior hypothalamus to the increased renal sympathetic nerve activity and decreased urinary sodium excretion resulting from environmental stress (air jet) in conscious spontaneously hypertensive rats were examined. Air stress increased mean arterial pressure and renal sympathetic nerve activity (54% from 7.0 ± 0.7 integrator resets/min), and decreased urinary sodium excretion (44% from 2.7 ± 0.4 ^Eq/min per 100 g body weight). After bilateral injection of ICI 118,551 OS2-adrenoceptor antagonist) into the posterior hypothalamus of the same spontaneously hypertensive rats, air stress had no effect on renal sympathetic nerve activity (8% from 4.8 ± 0.7 integrator resets/min) or urinary sodium excretion (2% from 5.2 ± 0.8 /lEq/min per 100 g body weight), but still increased mean arterial pressure. Bilateral injection of isoproterenolol (/9-adrenoceptor agonist) into the posterior hypothalamus enhanced the renal sympathetic nerve activity and urinary sodium excretion (but not mean arterial pressure) responses to air stress. Air stress had no effect on renal sympathetic nerve activity or urinary sodium excretion when ICI 118,551 was given into the posterior hypothalamus before isoproterenol. Atenolol (/Ji-adrenoceptor antagonist) had no effect on the renal responses to air stress when given alone or before isoproterenol. Similarly, ICI 118,551 administered into the lateral hypothalamus or lateral cerebral ventricle, or guanabenz (a 2 -adrenoceptor agonist) given into the posterior hypothalamus, had no effects on the renal or mean arterial pressure responses to air stress. Thus, /3 2 -adrenoceptors in the posterior hypothalamus mediate the increased renal sympathetic nerve activity and antinatriuresis resulting from environmental stress in conscious spontaneous hypertensive rats. (Circ Res 58: 241-248, 1986)

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Effects of catecholamines injected into the septal area of the rat brain on natriuresis, kaliuresis and diuresis

Cited by 40 publications

References 1 publication

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

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

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

Hypothalamic beta 2-adrenoceptor control of renal sympathetic nerve activity and urinary sodium excretion in conscious, spontaneously hypertensive rats.

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