Publications by authors named "Bakhramov A"

Hypoxic pulmonary vasoconstriction (HPV) may be mediated, in part, by an oxygen-sensing mechanism intrinsic to pulmonary arterial smooth muscle. It has been proposed that hypoxia inhibits a K+ conductance, which promotes membrane depolarization, subsequent activation of L-type Ca2+ channels and ultimately constriction. We have monitored hypoxia-induced changes in the intracellular Ca2+ concentration ([Ca2+]i) of single myocytes isolated from the rat pulmonary arterial tree using microspectrofluorimetry and ratiometric measurement of indo-1 fluorescence.

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Simultaneous patch-clamp and Ca2+ fluorescence measurements have revealed depolarising oscillations in the membrane potential of arterial (pulmonary) myocytes in response to adenosine 5'-triphosphate (ATP) and endothelin-1 (ET-1). These oscillations (i) are due to the preferential activation of Ca(2+)-activated Cl-, over K+ currents, (ii) occur through a mechanism involving Ca2+ release from intracellular Ca2+ stores and (iii) are likely to promote constriction. These results provide a novel perspective into the relative contribution and importance of Ca2+ activated Cl- and K+ channels in controlling membrane potential of arterial smooth muscle in response to contractile agonists.

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1. Calcium-induced transient inactivation of NMDA receptor (NMDAR) channels was studied in cultured rat hippocampal and cerebellar granule neurones using patch-clamp techniques and confocal scanning microscopy. 2.

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1. Single smooth muscle cells from the longitudinal muscle layer of guinea-pig small intestine were voltage clamped in the whole-cell recording mode with patch pipettes. The cationic current (Icat) evoked by application of 50 microM carbachol (CCh) was examined when free internal calcium in the cell was 'clamped' at 10(-7) M with 20 mM BAPTA.

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Cultured astrocytoma cells were voltage clamped with pipettes where [Ca2+] in the pipette was buffered to 10(-7) M with 10 mM 1,2-bis(O-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid (BAPTA) and membrane currents recorded. In isotonic solution predominantly K+ currents were evoked by depolarizing or hyperpolarizing commands and 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS; 1 mM) had little effect on inward and outward currents evoked by voltage steps to negative and positive potentials. If the osmolarity of the bathing solution was reduced from 280 to 200 mosmol l-1, a large current developed, which rectified outwardly and reversed close to the equilibrium potential for chloride ions, ECl.

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The whole cell patch clamp technique was used to study the effects on membrane currents of infection of cultured human embryonic lung (HEL) fibroblasts with human cytomegalovirus (CMV). Four types of membrane currents were found in uninfected HEL cells, namely: Ca(2+)-activated potassium current, inward rectifier potassium current, delayed rectifier potassium current and voltage-dependent CMV. Voltage-dependent sodium current was detected in 30% of uninfected HEL cells whenever they were examined up to 72 h after seeding; however this current had completely disappeared by 18 h after infection with CMV.

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The conductance of pores induced by Staphylococcus aureus alpha-toxin in Lettre cells has been compared to that in bilayers composed of synthetic lipids or Lettre cell membrane constituents. Previously described characteristics of toxin-induced conductance changes in lipid bilayers, namely rectification, voltage-dependent closure, and closure at low pH or in the presence of divalent cations (Menestrina, 1986) are displayed also in bilayers prepared from Lettre cell membranes and in patch clamped Lettre cells. It is concluded that endogenous proteins do not affect the properties of alpha-toxin-induced channels significantly and that the relative lack of ion channels in Lettre cells makes them ideal for studies of pore-forming toxins by the patch clamp technique.

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1. The membrane response to applied histamine of cultured endothelial cells from human umbilical vein was studied by use of whole cell and single channel patch clamp techniques. A value of -27 +/- 1.

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The role of A. laidlawii membrane lipids in the organism's interaction with mouse spleen lymphocytes is analyzed. A.

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The interaction of Acheleplasma laidlawii cells, derived membranes and liposomes with mouse spleen lymphocytes does not require the energy and participation of electrostatic coupling. The absence of pinocytosis of mycoplasma is demonstrated. Specific membrane receptors don't participate in mycoplasma and lymphocyte binding.

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