Increased sodium appetite in the rat induced by intracranial administration of components of the renin‐angiotensin system.

Avrith, D. B.; Fitzsimons, J. T.

doi:10.1113/jphysiol.1980.sp013210

Cited by 151 publications

(55 citation statements)

References 13 publications

(21 reference statements)

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“…Intracranial injection of Ang II stimulates the neural activity of sCVOs and induces water and salt intake (Buggy and Fisher 1974;Avrith and Fitzsimons 1980;Rowland et al, 1996;Sunn et al, 2003). Previous studies reported that some neurons in the sCVOs, where AT1a is abundantly expressed, are activated by systemic Na depletion (Fitzsimons, 1998) and that the neural activities in Na-depleted animals are supressed by intracerebroventricular injection of AT1a antagonists along with the reduction of salt-intake behaviors .…”

Section: Ii1 Introductionmentioning

confidence: 99%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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Section: Ii1 Introductionmentioning

confidence: 99%

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

et al. 2016

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“…The possible role of angiotensin in sodium appetite is less clear. There is good evidence that angiotensin infused directly into the brain stimulates sodium appetite (Avrith & Fitzsimons, 1980;Bryant, Epstein, Fitzsimons & Fluharty, 1980). However, unless there is a coexisting hypovolaemia, presumably providing a neural signal to sodium appetite, circulating angiotensin seems rather ineffective at stimulating increased intake of NaCl.…”

Section: Discussionmentioning

confidence: 99%

Increased sodium appetite and polydipsia induced by partial aortic occlusion in the rat.

Costales¹,

Fitzsimons²,

Vijande³

1984

The Journal of Physiology

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SUMMARY1. Partly occluding the abdominal aorta between the renal arteries caused the rat to drink steadily increasing amounts of 2-7 % NaCl when this solution and water were available.2. The increase in NaCl intake preceded the increase in water intake that also occurred after aortic occlusion, and intakes of both fluids were reaching maximal values 1-2 weeks after operation. 3. The amounts of fluid drunk during the day increased greatly. This change in the pattern of drinking, together with the rise in fluid intake and the drop in food intake meant that drinking was less associated with feeding than it is in the normal rat.4. The rats went into fluid and electrolyte deficit within 24 h of partial aortic occlusion and remained in deficit for about a week (the duration of the balance experiment) despite increasing intakes of NaCl and water.5. Renal function was unimpaired during the first 2 weeks, and the abnormal signs were mainly and rapidly reversed by removal ofthe ischaemic kidney or administration of the angiotensin converting enzyme inhibitor, captopril.6. Therefore polydipsia and increased sodium appetite in the first 2 weeks after aortic occlusion were likely to have been caused by fluid deficit, with increased renin secretion from the ischaemic kidney contributing to both behaviours.7. Arterial blood pressure rose immediately after aortic occlusion, before the onset of increased drinking. Up to 3 weeks after operation the incidence and severity of the hypertension did not appear to depend on the spontaneous changes in intake of water or hypertonic NaCl.

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“…In addition, repeated systemic injections of renin or of isoprenaline eventually produced the same moderate and consistent appetite for salt. When, in the subsequent experiments reported here, the hormone was infused continuously into the anterior third ventricle the appetite occurred in all animals and was never less than that seen after adrenalectomy despite the fact that all animals were probably in positive Na balance, as shown in the accompanying paper (Avrith & Fitzsimons, 1979), and in some rats was expressed in massive intakes of 3 0 % NaCl. At rates of 60 ng h-L to 6 jug h-1, 46 % of the animals drank at least 100 ml/day and 76 % drank at least 59 ml/day.…”

Section: Drinkometer Analysis Of Pattern Of Onsetmentioning

confidence: 99%

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

Bryant¹,

Epstein²,

Fitzsimons³

et al. 1980

The Journal of Physiology

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149

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SUMMARY1. Prolonged exposure of the brain of the normal Na-replete rat to angiotensin II produced a marked and persistent Na appetite. In a first series of experiments, short-term, repeated systemic injections of isoprenaline or renin (both of which raise circulating angiotensin levels), and repeated intracranial injections of angiotensin II evoked increased ingestion of 2-7 % NaCl. In the second series of experiments, continuous infusions of angiotensin II directly into the brain evoked extremely large intakes of 3 % NaCl.2. In addition to large intakes of hypertonic NaCl some rats drank daily volumes of water that exceeded their body weight.3. Not only did the animals drink large volumes of 3 % NaCl during continuous angiotensin II infusion, but after termination of the infusion they continued to ingest NaCl at a rate comparable to that of the adrenalectomized rat. In most of the animals the persistent NaCl intake diminished over several days, but other animals continued to drink NaCl for as long as their intake was measured (up to 7 months).4. The response to continuous infusion of angiotensin II was dose-dependent.Both water and 3 % NaCl intake increased over a dose range of 6 ng h-1 to 6000 ng h-1.The persistence of the sodium appetite was also dose-dependent across the same range of doses. 5. Angiotensin-induced salt appetite is specific for Na. Animals did not drink 0.5 M-NH4CI and only occasionally drank minimal amounts of 0 5 M-KCl during continuous infusion. 6. The large water turnover was not responsible for the Na appetite. Rats given access to 3 % NaCl only during infusion of angiotensin drank copiously. Animals that were not infused but were given saccharine-flavoured water in order to increase their water intakes did not drink 3 % NaCl offered at the same time even though fluid intake was high. Rats that did not receive intracranial infusions but were infused intragastrically with volumes of water equal to or exceeding the amounts that were drunk during angiotensin infusion did not drink the 3 % NaCl but did drink some water.

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Increased sodium appetite in the rat induced by intracranial administration of components of the renin‐angiotensin system.

Cited by 151 publications

References 13 publications

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Distinct neural mechanisms for the control of thirst and salt appetite in the subfornical organ

Increased sodium appetite and polydipsia induced by partial aortic occlusion in the rat.

Arousal of a specific and persistent sodium appetite in the rat with continuous intracerebroventricular infusion of angiotensin II.

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