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Biomedical subjects

E Tarjan

Publications and source records attributed to E Tarjan.

43 records · Page 3Linked to original sources
PubMed1982

Role of sodium concentration of the cerebrospinal fluid in the salt appetite of sheep.

The role of sodium concentration of the cerebrospinal fluid (CSF[Na]) in the initiation and/or satiation of Na appetite of Na-deplete or Na-replete sheep was investigated. Slow infusion (1 ml/h) into a lateral brain ventricle of an artificial sheep CSF solution was begun 0-60 min prior to and continued until the end of the Na access period (30-120 min). In Na-deficient sheep, increasing CSF[Na] caused a decrease in Na intake. In both Na-deficient and Na-replete sheep, decreasing CSF[Na] caused an increase in Na intake. The appetite was observed within 25 min of beginning infusion, which represents the most rapid induction of Na appetite yet observed. In Na-replete sheep, the appetite induced by decreasing CSF[Na] was predominantly for Na-containing solutions. A decrease in CSF[Na] of only 4-6 mmol/l was sufficient to induce Na appetite. The results derived by use of different Na, saccharide, or urea containing artificial CSF solutions suggest that there are sensors within the neuropil that respond to change of [Na] and influence salt appetite. They can be accessed by inducing change in [Na] of cerebroventricular CSF.

Animals↗
PubMed1981

Sodium appetite in sheep induced by cerebral ventricular infusion of angiotensin: comparison with sodium deficiency.

Intraventricular administration of supraphysiological amounts of renin, nerve growth factor preparation, or angiotensin II greatly increased the consumption of water and hypertonic sodium bicarbonate solution by sheep. These effects were antagonized by intraventricular administration of drugs that prevent the formation of angiotensin II or block its receptors. The fact that these angiotensin-blocking drugs did not change the sodium intake of sodium-deficient sheep challenges the idea that central angiotensin action is involved in sodium appetite due to a deficiency.

Angiotensin II↗
PubMed1981

Influence of mannitol-induced reduction in CSF Na on nervous and endocrine mechanisms involved in the control of fluid balance.

Infusions (20 microliter/min) of isotonic (0.27 M) and hypertonic (0.7 M) mannitol dissolved in Na-free artificial CSF were made for 1 h. into the lateral cerebral ventricle (IVT) of conscious water-replete sheep. The IVT infusion of both 0.27 M and 0.7 M mannitol induced a water-diuresis. Samples of CSF were collected prior to, and 5, 35, 65, 125 min after the end of the infusion. These consistently showed a reduction in CSF [Na], while CSF osmolality remained unchanged after 0.27 M mannitol, and was considerably increased after 0.7 M mannitol. In the 44 dehydrated sheep IVT infusion of 0.7 mannitol in Na-free artificial CSF was made for 6 h. The water deprivation as such caused a marked increase in plasma and CSF [Na] and osmolality. The 6 h IVT infusion of hypertonic mannitol further increased the CSF osmolality, while CSF [Na] decreased and reached a values below the normal for water-replete animals. The infusion also induced a fall in plasma ADH resulting in a water-diuresis, and extinguished the thirst of the dehydrated sheep. Furthermore, the infusion markedly reduced renal sodium excretion with causing any substantial change in blood aldosterone, in spite of the fact that there was a conspicuous increase in plasma renin concentration. The study supports the view that sodium sensitive receptors close to the cerebral ventricular system participate in the regulation of ADH secretion, water intake, renin release, and renal sodium excretion.

Animals↗
PubMedDate not supplied

Water and sodium intake of wild and New Zealand Rabbits following angiotensin.

Two rabbit strains, New Zealand (laboratory) rabbits and Australian wild rabbits, both members of the Oryctolagus cuniculus genus were studied. New Zealand rabbits under control conditions consumed 2-5 times more water and 8-30 times more 0.5 M NaCl/kg body weight than wild rabbits. Single injections of angiotensin II or III administered ICV did not induce water drinking in either strain. Acute ICV infusion of angiotensin II also did not influence water intake, but after several days of administration, induced increased sodium intake. Intravenous infusion of graded doses of angiotensin II induced diuresis only at the higher doses in both strains. In New Zealand rabbits, this was accompanied by a commensurate and concurrent increase in water intake. Intravenous infusion of angiotensin II also induced urinary sodium loss that was either accompanied or followed by increased sodium intake. The development of salt appetite in both strains was preceded by sodium loss.

Angiotensin II↗