On some electrolytic and water metabolism modifications in rats susceptible to audiogenic convulsions.
Following our research in the relationship between mechanisms of blood transportation of sodium and cerebral excitability, we studied adult rats (males-180-230 gm), divided into two groups according to their level of excitability to noise: 1. Rats susceptible to audiogenic convulsions and, 2. Rats with normal response to acoustic stimulation. In the two groups we determined the following parameters: 1. mechanisms of blood transportation of sodium; 2. general free motor behaviour; oriented behaviour (to satisfy motivation for sodium or water); nature and intensity of motivation expressed as milliliters of liquid and grams of sodium consumed; 3. influence of the variable sodium intake on the renal elimination of sodium, potassium and water. Also the influence of the variable water intake on the renal elimination of water. Results obtained show that: cerebral hyperexcitability manifested as susceptibility to audiogenic convulsions is associated with several modifications expressed as follows: 1) Sodium transportation in blood serum occurs in a free state in rats susceptible to audiogenic convulsions, while in normal rats it occurs in a state of interaction with serum proteins; 2) In animals susceptible to audiogenic convulsions one can notice significant hypermotricity in the behaviour cage; 3) Hyperexcitable animals consume significantly more sodium chloride solution which they freely choose, in a motivational manner, than animals with a normal excitability; 4) Increased, motivational consumption of sodium chloride is associated with increased renal elimination of sodium in animals susceptible to audiogenic convulsions. Increased renal elimination of sodium is accompanied by increased elimination of water, therefore with the protection of renal concentration mechanisms; 5) If we take the Na/K ratio as an indicator for the function of the corticosuprarenal and represent it as a function of the sodium intake, the data presented show that ratio is greater in animals with cerebral hyperexcitability, which is in concordance with the data presented, also involving the mineralcorticoid hormones in this response, a similar picture to that of loading the body with sodium; 6) The data presented seem to advocate once more for the idea that normal cerebral excitability is compatible with the existence of mechanisms that transport sodium in a state of oligoenergetic interaction with blood proteins.
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Institute of Normal and Pathological Physiology D. Danielopolu.
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D000161:Acoustic Stimulation; D000818:Animals; D001692:Biological Transport; D004231:Diuresis; D004327:Drinking Behavior; D004573:Electrolytes / Q000378:metabolism*; D020022:Genetic Predisposition to Disease; D008297:Male; D009043:Motor Activity / Q000502:physiology; D009318:Natriuresis; D051381:Rats; D012016:Reference Values; D012640:Seizures / Q000235:genetics* / Q000378:metabolism*; D012964:Sodium / Q000097:blood; D012965:Sodium Chloride; D014867:Water / Q000378:metabolism*
D004573:Electrolytes; D014867:Water; D012965:Sodium Chloride; D012964:Sodium