[Na+] of lateral ventricular cerebrospinal fluid in conscious rabbits before and after osmotic and hypovolemic stimuli

Kapsha, J.M.; Keil, L. C.; Severs, Walter B.

doi:10.1016/0014-4886(82)90165-0

Cited by 9 publications

(4 citation statements)

References 20 publications

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“…The c.s.f. sodium concentration in wild rabbits was 147-148 mm, similar to that of New Zealand rabbits (Kapsha, Keil & Severs, 1982). The measured sodium concentration in the third ventricular c.s.f.…”

Section: Discussionsupporting

confidence: 75%

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Denton¹,

Nelson²,

Tarján³

1985

The Journal of Physiology

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SUMMARY1. Wild rabbits trapped in their natural habitat and adapted to laboratory conditions were studied. Food, water and electrolyte (0-5 M-NaCl, 0-5 M-KCl, 0-25 M-MgCl2 and 0-25 M-CaCl2) consumption, urinary volume and sodium losses were monitored daily following stimuli which were found dipsogenic in other species.2. Water drinking was observed immediately after the intravenous injection of 1 M-NaCl (3 ml/kg), and following withdrawal of a mean of 13-9 % of calculated blood volume. Daily intake of water decreased during intracerebroventricular (i.c.v.) infusion of 0 3 M-NaCl in artificial cerebrospinal fuid (c.s.f.), during i.c.v. infusion of 0 9 M-mannitol c.s.f., both at a rate of 17 1d/h, following peritoneal dialysis with 5 % (w/v) glucose solution, and during food restriction. Water intake was not affected following intravenous administration of acetazolamide (10 mg/kg).3. Daily intake of 0'5 M-NaCl solution was increased following peritoneal dialysis with 5 % (w/v) glucose solution, which caused hyponatraemia, but not after haemorrhage which caused about the same sodium deficit as peritoneal dialysis, but as an isosmotic loss. 4. Administration of two different angiotensin II analogues, systemically or i.c.v., failed to induce water drinking. However, urinary sodium excretion and intake of 05 M-NaCl were increased during the 5 days of i.c.v. infusion of angiotensin II (10 pmol/h). Infusion for 1 day of angiotensin II (500 pmol/h) led to increased urinary sodium excretion which was followed by increased intake.5. The intake of other electrolyte solutions was not significantly affected by any of the treatments detailed above.6. The mechanisms participating in initiation of thirst in wild rabbits are very sensitive to decrease in blood volume, in contrast to other species studied in laboratories. Angiotensin II at the doses and routes administered was not dipsogenic in wild rabbits.7. The increased intake of 05 M-NaCl solution observed during and after the long-term intraventricular administration of angiotensin II in the wild rabbit appears predominantly a response to sodium deficit caused by natriuresis. The persistence of appetite after the cessation of infusion is indicative of a residual effect on central mechanisms of salt appetite.

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Section: Discussionsupporting

confidence: 75%

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Denton¹,

Nelson²,

Tarján³

1985

The Journal of Physiology

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“…Most previous investigators have found CSF sodium concentrations to be from 5 to 6 meq/1 higher than plasma levels. This has been most recently reported in both conscious rabbits 30 and dogs. 31 The mechanisms responsible for these differences are not well understood.…”

Section: Discussionmentioning

confidence: 89%

Sequential changes of cerebrospinal fluid sodium during the development of hypertension in Dahl rats.

1989

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The role of sodium retention and consequent changes in cerebrospinal fluid sodium concentration in the genesis of hypertension in Dahl rats was evaluated. Dahl salt-sensitive (DS, it=7), Dahl salt-resistant (DR, n=7), and Sprague-Dawley (n=6) rats were housed in metabolic cages and instrumented with a stainless steel cannula in the cisterna magna and a femoral arterial catheter. A blood sample was drawn daily (200 fit), and cerebrospinal fluid was collected by continuous 24-hour withdrawal (200 /til/day). Daily sodium, potassium, and water balances were also determined. Rats were studied sequentially on 0.4%, 4%, and 8% sodium diets (7 days per sodium level). Mean arterial pressure increased with 4% NaCI from 107 to 120 mm Hg (p<0.05) over 24 hours in DS rats and remained at about that level until the NaCI was increased to 8 %, which resulted in a gradual rise of mean arterial pressure over the next 7 days to 135 mm Hg. Cerebrospinal fluid sodium was unchanged in DR and Sprague-Dawley rats fed 4% or 8% sodium, but in DS rats rose from 152.3 to 155.2±0.6 meq/1 on the third day at 4% sodium and remained elevated over the next 2 weeks of study. Blood sodium was unchanged throughout the study in all groups. On the first day only of the 4% and 8% sodium diets, both DS and DR rats exhibited a similar net retention of sodium, which was greater than the Sprague-Dawley rats (p<0.05). There was no evidence for greater retention of sodium or water, however, in DS rats compared with DR or Sprague-Dawley rats when subjected to a high sodium diet. In summary, since mean arterial pressure rose in DS rats on the first day of the 4% sodium diet while cerebrospinal fluid sodium did not change until the third or fourth day, we conclude that these central changes were not the stimulus for the initial rise of arterial pressure but might contribute to the maintenance of the hypertension. (Hypertension 1989; 13:243-249) D ahl salt-sensitive (DS) and salt-resistant (DR) rats have been studied by many investigators interested in the phenomenon of sodium-dependent hypertension.12 These studies have yielded useful information related to the cardiovascular factors and renovascular abnormalities associated with the established phase of hypertension after 6-8 weeks of a high sodium diet.2 It has been shown that DS rats have an impaired renal capacity to excrete sodium, even before exposure to a high salt diet and subsequent hypertension. This renal impairment appears to be related to an intrinsic alteration of renal excretory function since cross-transplantation of kidneys from DS rats to DR rats transfers the salt-sensitive characteristic to the

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“…In rats (31) and other species (24,36), [Na ϩ ] is higher in the CSF than in plasma. Na ϩ transport across the blood-brain barrier (BBB) from the plasma to the CSF may depend on 1) epithelial sodium channels (ENaC) at the inner surface of the endothelial membrane of brain capillaries (39), including those at the choroid plexus, and probably at the epithelium covering the choroid plexus; and 2) Na ϩ -K ϩ -ATPase at the outer surface of the brain capillaries (1) and at the CSF side of the choroidal epithelium (22).…”

mentioning

confidence: 98%

Increases in CSF [Na⁺] precede the increases in blood pressure in Dahl S rats and SHR on a high-salt diet

Huang¹,

Vliet²,

Leenen³

2004

American Journal of Physiology-Heart and Circulatory Physiology

131

145

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In Dahl salt-sensitive (S) and salt-resistant (R) rats, and spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats, at 5-6 wk of age, a cannula was placed in the cisterna magna, and cerebrospinal fluid (CSF) was withdrawn continuously at 75 microl/12 h. CSF was collected as day- and nighttime samples from rats on a regular salt intake (0.6% Na+; R-Na) and then on a high salt intake (8% Na+; H-Na). In separate groups of rats, the abdominal aorta was cannulated and blood pressure (BP) and heart rate (HR) measured at 10 AM and 10 PM, with rats first on R-Na and then on H-Na. On H-Na, CSF [Na+] started to increase in the daytime of day 2 in Dahl S rats and of day 3 in SHR. BP and HR did not rise until day 3 in Dahl S rats and day 4 in SHR. In Dahl R and WKY rats, high salt did not change CSF [Na+], BP, or HR. In a third set of Dahl S rats, sampling of both CSF and BP was performed in each individual rat. Again, significant increases in CSF [Na+] were observed 1-2 days earlier than the increases in BP and HR. In a fourth set of Dahl S rats, BP and HR were recorded continuously by means of radiotelemetry for 5 days on R-Na and 8 days on H-Na. On H-Na, BP (but not HR) increased first in the nighttime of day 2. In another set of Dahl S rats, intracerebroventricular infusion of antibody Fab fragments binding ouabain-like compounds (OLC) with high affinity prevented the increase in BP and HR by H-Na but further increased CSF [Na+]. Finally, in Wistar rats on H-Na, intracerebroventricular infusion of ouabain increased BP and HR but decreased CSF [Na+]. Thus, in both Dahl S and SHR on H-Na, increases in CSF [Na+] preceded the increases in BP and HR, consistent with a primary role of increased CSF [Na+] in the salt-induced hypertension. An increase in brain OLC in response to the initial increase in CSF [Na+] appears to attenuate further increases in CSF [Na+] but at the "expense" of sympathoexcitation and hypertension.

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[Na+] of lateral ventricular cerebrospinal fluid in conscious rabbits before and after osmotic and hypovolemic stimuli

Cited by 9 publications

References 20 publications

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Sequential changes of cerebrospinal fluid sodium during the development of hypertension in Dahl rats.

Increases in CSF [Na⁺] precede the increases in blood pressure in Dahl S rats and SHR on a high-salt diet

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[Na+] of lateral ventricular cerebrospinal fluid in conscious rabbits before and after osmotic and hypovolemic stimuli

Cited by 9 publications

References 20 publications

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Water and salt intake of wild rabbits (Oryctolagus cuniculus (L)) following dipsogenic stimuli.

Sequential changes of cerebrospinal fluid sodium during the development of hypertension in Dahl rats.

Increases in CSF [Na+] precede the increases in blood pressure in Dahl S rats and SHR on a high-salt diet

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Increases in CSF [Na⁺] precede the increases in blood pressure in Dahl S rats and SHR on a high-salt diet