Central AII evokes a normal sodium appetite in the Fischer rat, but its low spontaneous sodium intake may be related to reduced excitation and increased inhibition in septo-preoptic AII neurons

Falconetti, C.; Chapleur, Michèle; Fernette, Brigitte; Thornton, Simon N.

doi:10.1016/j.brainresbull.2003.10.009

Cited by 3 publications

(4 citation statements)

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“…The results reported here show that a low dose (0.5 mg ⁄ day for 3 days) of DOCA pretreatment of male Fischer rats failed to increase Ang II-induced 2% NaCl and water intake in conscious behaving rats but increased neuronal responsiveness to locally applied Ang II in the central forebrain region in urethane anaesthetised rats. The behavioural results are similar to those reported previously (19) indicating that, despite a reported decreased sensitivity to sodium depletion (15), the Fischer rat nonetheless responds to Ang II Aldo Ang II Glut Fig. 1.…”

Section: Discussionsupporting

confidence: 90%

“…Although salt appetite can be elicited by peripheral administration of Ang II, it appears to interact with central structures in the forebrain to produce its effect (21). In the results shown here, consummation of the hypertonic salt solution was slightly higher than that reported previously (19) where the rats had access to food with a normal sodium concentration. In these experiments, the lower salt concentration of the food would have motivated the rats to consume more of the salt solution.…”

Section: Discussioncontrasting

confidence: 81%

“…Ang II‐induced ingestion of water and sodium is thought to have a similar mechanism in all rats and so it is logical to consider that, if the responsiveness of Fischer rats to mineralocorticoids is decreased, then their behavioural responses to Ang II would be decreased. However, despite the suggestion of lowered responsiveness to central Ang II, we have shown previously that Fischer rats drink the same amount of water and salt solution in response to the central administration of Ang II compared to Wistar rats although the daily intake of salt was less (19). Thus, it would appear that the brain circuitry for salt intake in response to Ang II is intact but that to mineralocorticoids is reduced.…”

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confidence: 72%

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Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Omouessi

Falconetti

Chapleur

et al. 2006

J Neuroendocrinology

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Central administration of angiotensin (Ang) II stimulates thirst and sodium intake via the AT-1 receptor. Mineralocorticoid pretreatment enhances Ang II-induced drinking of hypertonic salt solutions (i.e. the synergy theory) in Wistar and Sprague-Dawley rats. Electrophysiological experiments using iontophoretic application of Ang II, and the AT-1 receptor specific nonpeptide antagonist losartan, have shown excitation of neurones in the preoptic/medial septum region of urethane anaesthetised male Wistar rats. Deoxycorticosterone acetate (DOCA) pretreatment further enhanced this neuronal excitation to Ang II and reduced the responses to losartan. This generated the hypothesis that DOCA-enhanced Ang II-induced neuronal excitation was necessary for the enhanced salt intake of synergy theory. We tested this hypothesis in Fischer 344 rats that are known to have a low basal salt appetite and reduced sensitivity for i.c.v. Ang II. We compared the effect of DOCA pretreatment on i.c.v. Ang II-induced water and 2% NaCl intake in behaving adult male, Fischer rats, as well as preoptic/medial septum region neuronal responses to Ang II and losartan, using a seven-barrelled micro-iontophoretic electrode sealed to a recording electrode in urethane anaesthetised, male Fischer rats. Two groups were used: one pretreated with DOCA (0.5 mg/day for 3 days) and the other comprising controls, treated with isotonic saline. Ang II applied iontophoretically increased activity in 31% of the spontaneously active neurones. Following DOCA pretreatment, the responsiveness to Ang II (when applied after aldosterone) was increased. By contrast, in the behaving animals, water and 2% NaCl intake in response to i.c.v. Ang II were not enhanced by DOCA pretreatment. These results do not support the working hypothesis but could be interpreted as evidence for the existence of two separately modulated central Ang II systems: one responding to mineralocorticoids with increased neuronal activity and the other responsible for the Ang II-induced sodium appetite in conscious rats.

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Section: Discussionsupporting

confidence: 90%

Section: Discussioncontrasting

confidence: 81%

mentioning

confidence: 72%

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Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Omouessi

Falconetti

Chapleur

et al. 2006

J Neuroendocrinology

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“…Using the electrophysiological approach with iontophoretic application we observed that neurons in the forebrain of these rats were much less responsive to locally applied AngII than in Wistar rats (21). Furthermore, local application of losartan produced inhibition only and never excitation, as has been observed in Wistar rats (8,17).…”

mentioning

confidence: 80%

Mineralocorticoid modulation of central angiotensin-induced neuronal activity, water intake and sodium appetite

Thornton

Omouessi

Falconetti

2007

Braz J Med Biol Res

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Central angiotensin II (AngII) stimulates water and salt solution intake. Pretreatment with low-dose mineralocorticoid (DOCA) enhances this AngII-induced intake of salt solutions (the synergy theory) in Wistar and Sprague Dawley rats but not in Fischer rats. This response is mediated via the AT-1 receptor. Electrophysiological experiments using iontophoretic application of AngII and the AT-1 receptor-specific non-peptide antagonist losartan showed excitation of neurons in the preoptic/medial septum region of urethane-anesthetized male Wistar rats. DOCA pretreatment further enhances this neuronal excitation in response to AngII and reduces the responses to losartan. This generated the hypothesis that DOCA-enhanced AngIIinduced neuronal excitation is the neural support for the synergy theory. AT-2 receptors modulate these intake responses depending on sodium in the diet, and diuretic-induced dehydration during pregnancy produces a higher salt intake in the offspring. AngII-induced salt and water intakes were tested in offspring from Sprague Dawley mothers with only 1.8% NaCl to drink in which half were treated with furosemide. The important observations were a) the AT-1 antagonist alone suppressed intakes in offspring from mothers not treated with furosemide, b) both AT-1 and AT-2 antagonists suppressed intakes in offspring from furosemide-treated mothers, and c) combined administration of AT-1 and AT-2 antagonists greatly suppressed water intake in offspring from mothers not treated with furosemide. These results suggest that AT-1 and AT-2 receptors have variable properties (receptor number and/or second messengers). Furthermore, the activity and function of these central AngII receptors depend on the background mineralocorticoid levels. The exact mechanism of this influence, however, remains to be determined. Correspondence

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Gender and obesity influence sodium intake and fluid regulation in Zucker rats following repeated sodium depletions

Omouessi

Chapleur

Leshem

et al. 2006

Physiology & Behavior

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Central AII evokes a normal sodium appetite in the Fischer rat, but its low spontaneous sodium intake may be related to reduced excitation and increased inhibition in septo-preoptic AII neurons

Cited by 3 publications

References 36 publications

Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Mineralocorticoid Pretreatment Enhances Angiontensin II‐Induced Neuronal Excitation But Not Salt Drinking in Male Fischer Rats

Mineralocorticoid modulation of central angiotensin-induced neuronal activity, water intake and sodium appetite

Gender and obesity influence sodium intake and fluid regulation in Zucker rats following repeated sodium depletions

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