Acta physiologica Academiae Scientiarum Hungaricae最新文献

Effects of intraperitoneal administration of cholecystokinin (CCK)-related peptides were studied on retention of single-trial learning passive avoidance behaviour. The COOH-terminal octapeptide of CCK (CCK-1-8-SE), the unsulfated octapeptide (CCK-1-8-NS), as well as the COOH-terminal tetrapeptide of CCK (CCK-5-8), administered immediately after the learning trial, facilitated passive avoidance behaviour. The data indicate that these peptides may influence memory consolidation processes.

The coronary vascular effect of various divalent cations and of sodium-metavanadate was compared in isolated perfused rat hearts. Their order of activity was as follows (the concentrations (microM) evoking a half-maximum increase of coronary resistance are indicated (in parentheses): Ni2+ (0.03) greater than Co2+ (0.1) greater than Hg2+ (0.16) greater than VO-3 (0.2) greater than Cu2+ (15) greater than Zn (50). Iron (Fe2+) and cadmium (Cd2+) were ineffective. The order of coronary vasoconstrictor potency of these metal ions differs from the order of their other physico-chemical properties indicating that their coronary action cannot be explained as being singly a consequence of ion-membrane interaction. In contrast to Ni2+, the effect of Hg2+ was totally inhibited by phenoxybenzamine (10(-5)M) indicating that coronary vasoconstriction induced by mercury ions is mediated by alpha-receptors. Coronary vasoconstriction induced by sodium-meta-vanadate was resistant to verapamil while removal of external Ca2+ potentiated its effect. These data suggest that in contrast to Ni2+ and Hg2+, vanadate increases coronary resistance by mobilizing intracellular Ca2+ in vascular smooth muscle cells.

Differential distribution of gross, particulate and soluble forms of hexokinase in the cerebrum, cerebellum, pituitary, hypothalamus and thalamus and medulla oblongata was studied in 9 inland teleosts of different phylogenetic age to clarify the compartmentation of glucose metabolism. Enzyme activity (gross) was maximum in the cerebrum and minimum in the medulla oblongata, suggesting that glucose metabolism is more intensive in the former structure. The activity in the particulate fraction was highest in the cerebellum followed by the cerebrum, midbrain and medulla oblongata. Gross, particulate and soluble fraction of the enzyme was higher in major carp species than in cat fish or snake head species. Total particular and soluble fraction was highest in the cerebrum, cerebellum and midbrain. The distributional trend of the enzyme was similar in the 9 fishes.

Computer modelling technique is proposed to assist in physiological research on invertebrate neuronal membranes. The firing mechanism of a single patch of invertebrate neuronal membrane has been studied in dependence on maximum Ca++ conductance. The calculations are based on modification of Hodgkin-Huxley's data completed by a straight line approximation between experimental points of the kinetic parameters of Ca++ current and early transient potassium current. The time course of conductance changes is assumed to be proportional to m2h for Ca++ current. Three distinct potassium currents are involved into the model, viz. transient potassium current, delayed potassium current and Ca++-dependent potassium current. The modified Euler method run on a digital computer has been used for numerical integration of kinetic equations. Significant effects of Ca++ conductance on spike broadening, plateau development and spike afterhyperpolarization are represented. In the range of small Ca++ conductance an infinite spontaneous activity can be triggered by a short (suprathreshold) current pulse which may be considered a model of pacemaker activity. Plateau development resulting from potassium blocking or decreasing potassium equilibrium is facilitated by Ca++ conductance in the range of greater Ca++ conductance. The effects of voltage sensitivity of the coupling coefficient describing the current of Ca++-dependent K+ channels were studied and compared to the voltage independent case. The coupling coefficient seems to be a crucial factor in broadening the range of Ca++ conductance responsible for pacemaker activity. For greater values of Ca++ conductance, a decrease of the coupling coefficient leads to a transition from prolonged bursting to interruption of burst activity by burst-afterhyperpolarization. The blocking effect of 4-aminopyridine on fast outward current has been studied by the model which has a practical significance considering that aminopyridine is known as a convulsive agent. We suppose that it is reasonable to study the convulsive effects of aminopyridine by the model based on the kinetics of the isolated neuronal membrane. The model may help in understanding the ionic background underlying abnormal network activity during epileptic discharges of mammalian neurones.

In control and capsaicin-treated (300 mg/kg) rats tail skin vasodilatation was studied while the body temperature was raised to 38 degrees C, 39 degrees C or 40 degrees C and held at these levels. In the capsaicin-treated rats, at 38 degrees C vasodilatation was weaker than in the controls but at temperatures of 39 degrees C and 40 degrees C a delayed increase in tail vasodilatation occurred to the level observed in the controls. It is concluded that the threshold of vasodilatation response to heat is elevated after capsaicin treatment.

Low body weight premature babies born before the 32nd gestational week were studied to analyse the postnatal fall in plasma haemoglobin and in quantitative changes in amino acid levels. Red blood cells of premature low body weight infants were found to disintegrate more rapidly than those of mature newborns. Thin-layer ion-exchange chromatographic studies showed that amino acids originating from the degrading haemoglobin-F lead to rise in plasma amino acids. These amino acids might play a role as substrates for gluconeogenesis in the energy supply of low body weight premature babies during the special fasting state just after birth.

The unknown enzymatic mechanism of enhanced protein breakdown in steroid myopathy was studied in functionally and biochemically different muscles of rabbits treated with dexamethasone for three weeks. After glucocorticoid administration the fast-twitch glycolytic semimembraneous muscle of treated animals was atrophied, whereas the weight of the slow-twitch oxidative soleus muscle was not altered. The specific activity of the lysosomal endo- and exopeptidases (cathepsin D, E, B and L, lysosomal carboxypeptidase A and dipeptidylpeptidase I) was increased about 2-fold in the atrophied white muscle. The activity of the cytosol enzyme Ca++-activated neutral proteinase was also elevated, whereas that of the other cytosol endopeptidase, chymotrypsin-like enzyme, was unaltered. The level of alanine aminopeptidase was only slightly increased. On the other hand, there were no unequivocal changes in protease activity in the soleus muscle. These findings are in agreement with the known differences in glucocorticoid-sensitivity of the various muscles. Our results suggest that the lysosomal proteolytic system and the Ca++-activated neutral proteinase may play an important role in the glucocorticoid-induced intracellular protein catabolism in muscle. The inhibitor capacities of cathepsin B and trypsin detectable in muscle cytosol were not altered after steroid treatment. Consequently, the increase in cathepsin B activity was not due to the loss of its inhibitor.

Results of this study showed that in a considerable number of patients with duodenal ulcer a globulin of the IgG class was responsible for the enhancement of HCl secretion. This secretagogue globulin appeared to combine directly with the H2 receptors of the parietal cells thereby increasing hydrochloric acid output without the formation of antigen-antibody complex.

The purpose of the present study was to investigate the changes of characteristic parameters of myocardial reactive hyperaemia that follow coronary artery occlusion for 10 sec and of the coronary vascular response to hypoxia during constant verapamil infusion (0.01 mg. kg-1 X min-1) in anaesthetized open-chest dogs. Reactive hyperaemia was significantly reduced by the specific Ca-antagonist verapamil, while augmentation of coronary blood flow by 100% N2 inhalation for 30 sec was not significantly influenced by the drug. The experimental results indicate that, similar to myocardial cells, verapamil reduces the oxygen requirement of vascular smooth muscle cells as well. The possibility exist that verapamil excludes factor(s) responsible for the disproportional overpayment of flow debt.