Drinking caused by Constriction of the Inferior Vena Cava in the Rat

Jt, Fitzsimons

doi:10.1038/204479a0

Cited by 37 publications

(3 citation statements)

References 5 publications

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“…This expectation was confirmed. Complete ligation of the abdominal inferior vena cava in the rat caused osmotically inappropriate drinking, but unexpectedly, it proved much less effective as a stimulus of drinking in the nephrectomized rat (Fitzsimons, 1964).…”

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confidence: 96%

The role of a renal thirst factor in drinking induced by extracellular stimuli

Fitzsimons¹

1969

The Journal of Physiology

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204

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SUMMARY1. Rats in normal fluid balance drank water 1-2 hr after complete ligation of the inferior vena cava either above or below the renal veins. At the same time there was a fall in urine flow and excretion of electrolyte, especially after caval ligation above the renal veins, so that the animals ended the initial 6 hr period in positive fluid balance.2. Caval ligation was relatively ineffective as a stimulus to drinking after bilateral nephrectomy, but was effective in rats made anuric by ureteric ligation.3. Rats subjected to caval ligation and offered a choice between water and 1l8 % saline (w/v) drank water, despite the increasing hypotonicity of the body fluids thereby resulting. 4. During the secondary polydipsia, which generally occurred on about the third day after caval ligation as renal function was recovering, there was an increased preference for 18 % saline.5. Constriction of the aorta above the renal arteries, or constriction of both renal arteries, also caused drinking, oliguria and the development of positive fluid balance.6. Constriction of the aorta below the renal arteries, or after nephrectomy, was ineffective as a stimulus to drinking.7. Saline extracts of renal cortex caused rats in normal water balance to drink. Activity was destroyed by boiling the extract for 10 min. Renal medullary and hepatic extracts were without effect on drinking.8. It proved impossible to separate dipsogenic and pressor activities of renal extracts during the different stages of fractionation which lead to the production of renin; disappearance of one activity was invariably accompanied by disappearance of the other.9. Dipsogenic and pressor actions were greater in nephrectomized rats than in normal rats. J. T. FITZSIMONS 10. Both extractable dipsogenic factor and extractable pressor activity were reduced by treating the rat with DOCA and saline for several weeks beforehand.11. The renal dipsogen therefore has similar properties to renin. It may prove to be identical with renin, particularly in view of the fact that angiotensin also stimulates drinking.12. Adrenalectomy did not affect drinking induced by renin or by caval ligation.13. It is concluded that the renin angiotensin system may play a role in the genesis of the thirst which follows certain extracellular stimuli.

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confidence: 96%

The role of a renal thirst factor in drinking induced by extracellular stimuli

Fitzsimons¹

1969

The Journal of Physiology

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204

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“…This is one of the better established roles for angiotensin and it is tempting to assume that the hormone may also be the intermediary in the arousal of the Na appetite. This is suggested by the observation (Fitzsimons, 1964) that caval ligation, a known releaser of renin, evokes a delayed appetite for 1.8 % NaCl, and was discussed by Fisher & Buggy (1975) who noted a tendency for increased intakes of isotonic saline solutions in rats receiving pulse injection of large doses of angiotensin into the cerebral ventricles. Intraventricular infusions of angiotensin have been shown to produce impressive intakes of 2'7 % NaCl (Buggy & Fisher, 1974;Fisher & Buggy, 1975), but the intakes did not occur with high reliability when 09 % saline solutions were used (Radio, Summy-Long, Daniels-Severs & Severs, 1972), and infusions lasting 8 h (Fisher & Buggy, 1975) were the longest reported.…”

Section: Introductionmentioning

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

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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“…a Role of the Kidney in Extracellular Thirst: the Renin-Angiotensin System In the rat ligation of the inferior vena cava, which reduces venous return to the heart and reduces arterial blood pressure, leads to a marked increase in water intake and a positive fluid balance due to decreased urine flow. If both kidneys are removed before ligation, water intake is significantly reduced (Fitzsimons, 1964(Fitzsimons, , 1969, which suggests that an essential thirst stimulus following caval ligation could be a reduction in blood pressure to the kidneys. In order to test this hypothesis, Fitzsimons reduced the pressure to the kidneys by partially constricting the renal arteries, and found that water intake increased.…”

Section: Extracellular Thirst Stimulimentioning

confidence: 99%