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  • Acetylated low density lipoprotein  (1)
  • Action potentials  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 348 (1993), S. 207-212 
    ISSN: 1432-1912
    Keywords: Macrophage ; Voltage-clamp ; Ionic current ; Low density lipoprotein ; Acetylated low density lipoprotein
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The aim of the present study was to search for electrophysiological effects of human lipoproteins on membrane currents in mouse peritoneal macrophages which had been cultured for 5 to 20 days. Whole-cell currents were recorded by using a voltage-clamp technique. Low density lipoprotein (LDL, 100 μg/ml) increased a slowly activating nonspecific cation current (iso) in the positive potential range to 244 ± 23% of the reference (test potential + 55 mV, n = 13, P 〈 0.005). Augmentation of current resulted out of a negative shift of the activation curve along the voltage axis (−22 mV) and an increase of maximally available current. Furthermore, LDL increased a rapidly activating outward current (ifo) at test potentials positive to the potassium equilibrium potential. At +55 mV ifo-amplitude increasedto 165 ± 14% ofreference (n = 16, P 〈 0.005). LDL-induced effects on ifo-current could be mimicked by application of the calcium ionophore A 23187 (1 μmol/l) which led to an increase of ifo-current to 161 ± 25% of the reference (test potential + 55 mV, n = 11, P 〈 0.005). Acetylated-LDL (100 μg/ml, 5–15 min) produced no significant effect on the membrane currents under investigation.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 334 (1986), S. 294-302 
    ISSN: 1432-1912
    Keywords: H-receptor agonists ; Antihistamines ; Mammalian heart ; Action potentials ; Voltage clamp
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Histamine-induced electrophysiological effects have been investigated in guinea-pig left atria, papillary muscles and rabbit AV-nodal preparations by means of intracellular recording of action potentials, slow responses in the presence of 27 mmol/l (K+)o and voltage clamp experiments. Differentiation of the H-receptor subtypes was performed by the use of the H2-selective agonists dimaprit and impromidine and the H1- and H2-selective antagonists dimetindene and cimetidine, respectively. The following results were obtained: 1. Histamine and the H2-agonists dimaprit and impromidine show similar actions on electrophysiological parameters of ventricular myocardium. Histamine at concentrations 〈1 μmol/l leads to a small increase in APD30 and APD90, but to a marked decrease at concentrations ≥ 1 μmol/l, whereas $$\dot V_{\max } $$ , resting potential and amplitude remain nearly unchanged. The effects on APD are completely blocked by cimetidine and not changed by dimetindene. Changes in action potential may be explained by an increase in slow inward current and outward currents as shown by voltage clamp experiments. 2. In left atria histamine increases APD30 and APD90, whereas there is only a minor increase in amplitude with no changes in $$\dot V_{\max } $$ and resting potential. These effects are completely reversed by the H1-antagonist dimetindene but not by cimetidine. IBMX decreases APD90 and does not potentiate the action of histamine. 3. $$\dot V_{\max } $$ of slow responses is increased in left atria by stimulation of H1-receptors and in papillary muscles by stimulation of H2-receptors. The results suggest that stimulation of atrial H1-receptors directly causes an increase in Ca-channel conductance. 4. Differentiation of the positive inotropic actions in left atria by means of TTX, diltiazem and vanadate suggests that histamine increases Ca-conductance but does not affect Na-dependent window current. 5. Histamine reduces AH-interval, increases $$\dot V_{\max } $$ of NH-cells and induces AV-arrhythmias at concentrations ≥ 1 μmol/l. The results indicate that these effects are due to stimulation of H2-receptors.
    Type of Medium: Electronic Resource
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