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EN
Four week old Wistar-Kyoto (WKY) rats were divided into two groups. The experimental group (n=7) was receiving a high sodium diet (3.28% Na+) and the control group (n=7) a normal sodium diet (0.22% Na+). After 8 weeks, subjects were chronically implanted with the lateral cerebral ventricle (LCV) cannulas and with the femoral artery catheters. Three series of experiments were carried out on the experimental and control groups. In each series mean arterial pressure (MAP) and heart rate (HR) were recorded for 10 min before and 30 min after the LCV infusion. In series 1 artificial cerebrospinal fluid (aCSF) was administered (2 mul/15 s). In series 2 AVP was infused (20 ng/2 mul aCSF/15 s). In series 3 V1a receptor antagonist (V1 ANT), d(CH2)5[Tyr(Me)2,Ala-NH29]AVP, was applied (80 ng/mul aCSF/15 s). There was no difference in baseline MAP and HR between the experimental and control groups. LCV infusion of aCSF had no effect on MAP and HR. LCV infusion of AVP produced a significant increase of MAP, which was greater in the group on the high sodium diet than in the group on normal sodium diet. The experimental group showed a longer hypertensive effect of centrally applied AVP in comparison to the control. LCV administration of V1 ANT did not exert a significant effect on circulatory parameters. These results suggest that the prolonged high sodium diet does not induce hypertension in WKY rats, but it enhances the pressor function of the central vasopressinergic system.
EN
Cell movement in the amoebae Dictyostelium discoideum has been examined in media differing in monovalent cation concentration (i.e. Na+ and K+). Under isotonic or even slightly hypertonic conditions, the cells move equally well in solutions in which either potassium or sodium ions dominate. However, in strongly hypertonic solutions the amoebae showed motility in a 2% potassium chloride solution, but remained motionless in a hypertonic 2% sodium chloride solution. This inhibition of D. discoideum amoebae movement in a hypertonic sodium chloride solution was fully reversible. Such behaviour corresponds to that of plant, fungi, and some invertebrate animal cells rather than protozoan or vertebrate cells. These observations suggest that studies using D. discoideum as a model for cell motility in vertebrate animal tissue cells should be considered with caution, and would seem to confirm the classification of cellular slime moulds as related rather to Fungi than to Protista. This also shows that the cell membrane models should consider the asymmetry in sodium /potassium ion concentrations found in vertebrate animal cells as one of various possibilities.
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vol. 58
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issue 3
165-175
EN
Depolarization of cultured astrocytes by KCl stimulated gamma-aminobutyric acid (GABA) release in a dose-dependent manner. At 60 mM KCl, the stimulatory effect was calcium- and sodium- independent, and was not altered by the presence of beta- alanine. The potassium-evoked GABA release was inhibited by furosemide and 4-acetamido-4'-isothiocyano- -2,2'-stilbene disulfonic acid (SITS), blockers of the chloride transporter across the plasma membrane, as well by chloride ion replacement with glucuronate. Other depolarizing agents, such as veratridine and ouabain, decreased basal GABA release; ouabain also inhibited the stimulatory effect of 60 mM KCl. The high K^+-induced GABA release may affect CNS excitability and may represent an important aspect of glial-neuronal interactions.
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