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  1. Article ; Online: Electrophysiological characterization of the activating action of a novel liposomal nitric oxide carrier on Maxi-K channels in pulmonary artery smooth muscle cells.

    Ivanova, Irina V / Melnyk, Mariia I / Dryn, Dariia O / Prokhorov, Vitalii V / Zholos, Alexander V / Soloviev, Anatoly I

    Journal of liposome research

    2021  Volume 31, Issue 4, Page(s) 399–408

    Abstract: The aim of this study was to establish the mechanisms of action of a novel liposomal nitric oxide (NO) carrier on large-conductance ... ...

    Abstract The aim of this study was to establish the mechanisms of action of a novel liposomal nitric oxide (NO) carrier on large-conductance Ca
    MeSH term(s) Animals ; Calcium/metabolism ; Large-Conductance Calcium-Activated Potassium Channels ; Liposomes ; Myocytes, Smooth Muscle/metabolism ; Nitric Oxide/metabolism ; Pulmonary Artery/metabolism ; Rats
    Chemical Substances Large-Conductance Calcium-Activated Potassium Channels ; Liposomes ; Nitric Oxide (31C4KY9ESH) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2021-01-08
    Publishing country England
    Document type Journal Article
    ZDB-ID 645173-1
    ISSN 1532-2394 ; 0898-2104
    ISSN (online) 1532-2394
    ISSN 0898-2104
    DOI 10.1080/08982104.2020.1863424
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: C

    Melnyk, Mariia I / Ivanova, Irina V / Dryn, Dariia O / Prylutskyy, Yuriy I / Hurmach, Vasyl V / Platonov, Maxim / Al Kury, Lina T / Ritter, Uwe / Soloviev, Anatoly I / Zholos, Alexander V

    Nanomedicine : nanotechnology, biology, and medicine

    2019  Volume 19, Page(s) 1–11

    Abstract: Possessing unique physical and chemical properties, ... ...

    Abstract Possessing unique physical and chemical properties, C
    MeSH term(s) Animals ; Dynamic Light Scattering ; Fullerenes/pharmacology ; Humans ; Ion Channel Gating/drug effects ; Kv Channel-Interacting Proteins/metabolism ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism ; Male ; Mice, Inbred BALB C ; Molecular Docking Simulation ; Muscle Contraction/drug effects ; Myocytes, Smooth Muscle/drug effects ; Myocytes, Smooth Muscle/metabolism ; Pulmonary Artery/cytology ; Rats, Wistar
    Chemical Substances Fullerenes ; Kv Channel-Interacting Proteins ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits
    Language English
    Publishing date 2019-04-11
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2183417-9
    ISSN 1549-9642 ; 1549-9634
    ISSN (online) 1549-9642
    ISSN 1549-9634
    DOI 10.1016/j.nano.2019.03.018
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Protein kinase C-dependent inhibition of BK(Ca) current in rat aorta smooth muscle cells following gamma-irradiation.

    Kizub, Igor V / Pavlova, Oleksandra O / Ivanova, Irina V / Soloviev, Anatoly I

    International journal of radiation biology

    2010  Volume 86, Issue 4, Page(s) 291–299

    Abstract: Purpose: The aim of this study was to estimate the effects of non-fatal whole-body gamma-irradiation on outward potassium plasma membrane conductivity in rat vascular smooth muscle cells (VSMC), and to identify underlying mechanisms.: Materials and ... ...

    Abstract Purpose: The aim of this study was to estimate the effects of non-fatal whole-body gamma-irradiation on outward potassium plasma membrane conductivity in rat vascular smooth muscle cells (VSMC), and to identify underlying mechanisms.
    Materials and methods: Rats were exposed to a 6 Gy dose irradiation from a cobalt(60) source. Whole-cell potassium current was measured in freshly isolated rat aorta smooth muscle cells using standard patch-clamp technique.
    Results: We have determined that whole-body ionising irradiation significantly inhibits whole-cell outward K(+) current in rat aortic VSMC obtained from irradiated rats 9 and 30 days after irradiation, and this inhibition appears to be increased throughout post-irradiation period. Using selective inhibitors of small conductance Ca(2+)-activated K(+) channels (SK(Ca)), apamin (1 microM), intermediate conductance Ca(2+)-activated K(+) channels (IK(Ca,)), charybdotoxin (1 microM) and a large conductance Ca(2+)-activated K(+) channels (BK(Ca)), paxilline (500 nM), we established that the main component of whole-cell outward K(+) current in rat aortic VSMC is due to BK(Ca). It is clear that on the 9th day after irradiation paxilline had only a small effect on whole-cell outward K(+) current in VSMC, and was without effect on the 30th day post-irradiation, suggesting complete suppression of the BK(Ca) current. The PKC inhibitor, chelerythrine (100 nM), effectively reversed the suppression of whole-cell outward K(+) current induced by ionising irradiation in the post-irradiation period of 9 and 30 days.
    Conclusions: The results suggest that irradiation-evoked inhibition of the BK(Ca) current in aortic VSMC is mediated by PKC. Taken together, our data indicate that one of the mechanisms leading to elevation of vascular tone and related arterial hypertension development under ionising irradiation impact is a PKC-mediated inhibition of BK(Ca) channels in VSMC.
    MeSH term(s) Animals ; Aorta, Thoracic/cytology ; Electric Conductivity ; Electrophysiology ; Gamma Rays ; Large-Conductance Calcium-Activated Potassium Channel alpha Subunits/metabolism ; Myocytes, Smooth Muscle/enzymology ; Myocytes, Smooth Muscle/metabolism ; Myocytes, Smooth Muscle/radiation effects ; Patch-Clamp Techniques ; Protein Kinase C/metabolism ; Rats ; Time Factors ; Whole-Body Irradiation
    Chemical Substances Large-Conductance Calcium-Activated Potassium Channel alpha Subunits ; Protein Kinase C (EC 2.7.11.13)
    Language English
    Publishing date 2010-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 3065-x
    ISSN 1362-3095 ; 0020-7616 ; 0955-3002
    ISSN (online) 1362-3095
    ISSN 0020-7616 ; 0955-3002
    DOI 10.3109/09553000903564042
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article: Ionizing non-fatal whole-body irradiation inhibits Ca2+-dependent K+ channels in endothelial cells of rat coronary artery: possible contribution to depression of endothelium-dependent vascular relaxation.

    Tishkin, Sergey M / Rekalov, Vladimir V / Ivanova, Irina V / MoreLand, Robert S / Soloviev, Anatoly I

    International journal of radiation biology

    2007  Volume 83, Issue 3, Page(s) 161–169

    Abstract: Purpose: The goal of this study was to evaluate the influence of ionizing irradiation on large conductance Ca2+-dependent potassium (BKCa) channels in rat coronary endothelial cells.: Materials and methods: Rats were exposed to a 6 Gy dose from a ... ...

    Abstract Purpose: The goal of this study was to evaluate the influence of ionizing irradiation on large conductance Ca2+-dependent potassium (BKCa) channels in rat coronary endothelial cells.
    Materials and methods: Rats were exposed to a 6 Gy dose from a cobalt60 source. Experimental design of this study comprised recording of contractile force using isolated rat aortic rings and whole-cell patch clamp techniques to study whole-cell potassium currents in isolated rat coronary artery endothelial cells.
    Results: It has been shown that outward potassium currents in endothelial cells 9 days after irradiation appear to be suppressed or even totally abolished. The reversal potential for these currents in irradiated cells was shifted to more positive values. Paxilline (500 nM), an inhibitor of BKCa channels, had no or only a negligible effect on irradiated cells. The experiments using isolated aortic rings demonstrated that both paxilline and irradiation significantly shifted the acetylcholine dependent concentration-relaxation response curve to the right. Irradiated tissues were insensitive to paxilline.
    Conclusion: The results suggest that non-fatal, whole-body gamma-irradiation suppresses large conductance, calcium-activated potassium channels, which control the driving force for Ca2+ entry and therefore Ca2+ dependent nitric oxide (NO) synthesis in endothelial cells. This may contribute, in part, to radiation-induced endothelium dysfunction and an increase in arterial blood pressure.
    MeSH term(s) Acetylcholine/pharmacology ; Animals ; Aorta, Thoracic/cytology ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/radiation effects ; Coronary Vessels/cytology ; Coronary Vessels/drug effects ; Coronary Vessels/radiation effects ; Dose-Response Relationship, Drug ; Endothelial Cells/drug effects ; Endothelial Cells/physiology ; Endothelial Cells/radiation effects ; Gamma Rays ; Male ; Membrane Potentials/drug effects ; Membrane Potentials/radiation effects ; Patch-Clamp Techniques ; Paxillin/pharmacology ; Potassium Channels, Calcium-Activated/antagonists & inhibitors ; Potassium Channels, Calcium-Activated/physiology ; Rats ; Rats, Wistar ; Vasodilation/drug effects ; Vasodilation/radiation effects ; Vasodilator Agents/pharmacology ; Whole-Body Irradiation
    Chemical Substances Paxillin ; Potassium Channels, Calcium-Activated ; Vasodilator Agents ; Acetylcholine (N9YNS0M02X)
    Language English
    Publishing date 2007-03-07
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3065-x
    ISSN 1362-3095 ; 0955-3002 ; 0020-7616
    ISSN (online) 1362-3095
    ISSN 0955-3002 ; 0020-7616
    DOI 10.1080/09553000601146931
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  5. Article: Ionizing radiation alters myofilament calcium sensitivity in vascular smooth muscle: potential role of protein kinase C.

    Soloviev, Anatoly I / Tishkin, Sergey M / Zelensky, Sergey N / Ivanova, Irina V / Kizub, Igor V / Pavlova, Alexandra A / Moreland, Robert S

    American journal of physiology. Regulatory, integrative and comparative physiology

    2005  Volume 289, Issue 3, Page(s) R755–62

    Abstract: Radiation exposure increases vascular responsiveness, and this change involves endothelial damage, as well as direct effects on vascular smooth muscle. In this study, we tested the hypothesis that myofilament Ca(2+) sensitivity in vascular smooth muscle ... ...

    Abstract Radiation exposure increases vascular responsiveness, and this change involves endothelial damage, as well as direct effects on vascular smooth muscle. In this study, we tested the hypothesis that myofilament Ca(2+) sensitivity in vascular smooth muscle is increased from single whole body gamma irradiation (6 Gy). We measured contractile responses from intact and permeabilized rat thoracic aortic rings combined with cytosolic Ca(2+) ([Ca(2+)](i)) measurements. The sensitivity to KCl and phenylephrine increased significantly in tissues from animals on the 9th and 30th days postirradiation compared with control. Irradiation also significantly increased Ca(2+) sensitivity in beta-escin permeabilized smooth muscle on the 9th and 30th days postirradiation. Inhibitors of protein kinase C, chelerythrine, and staurosporine, had no effect on the pCa-tension curves in control permeabilized tissues but significantly decreased Ca(2+) sensitivity in permeabilized tissues on the 9th and 30th days postirradiation. Phorbol dibutyrate (PDBu, 10(-7) M) increased Ca(2+) sensitivity in control skinned smooth muscle but was without effect in irradiated vascular rings. Simultaneous measurement of contractile force and [Ca(2+)](i) showed that myofilament Ca(2+) sensitivity defined as the ratio of force change to [Ca(2+)](i) significantly increased following gamma-irradiation. PDBu (10(-6) M) stimulation of intact aorta produced a sustained contraction, while the increase in [Ca(2+)](i) was transient. In irradiated tissues, PDBu-induced contractions were greater than those seen in control tissues but there was no elevation in [Ca(2+)](i). Taken together, these data strongly support the hypothesis that irradiation increases the sensitivity of vascular smooth muscle myofilaments to Ca(2+) and this effect is dependent on activation of protein kinase C.
    MeSH term(s) Actin Cytoskeleton/physiology ; Actin Cytoskeleton/radiation effects ; Animals ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/physiology ; Aorta, Thoracic/radiation effects ; Calcium/metabolism ; Calcium/physiology ; Capillary Permeability ; In Vitro Techniques ; Intracellular Membranes/metabolism ; Muscle, Smooth, Vascular/physiology ; Muscle, Smooth, Vascular/radiation effects ; Osmolar Concentration ; Potassium Chloride/pharmacology ; Protein Kinase C/physiology ; Rats ; Rats, Inbred WKY ; Vasoconstriction/physiology
    Chemical Substances Potassium Chloride (660YQ98I10) ; Protein Kinase C (EC 2.7.11.13) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2005-05-12
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
    ZDB-ID 603839-6
    ISSN 1522-1490 ; 0363-6119
    ISSN (online) 1522-1490
    ISSN 0363-6119
    DOI 10.1152/ajpregu.00748.2004
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  6. Article: Mechanisms of endothelial dysfunction after ionized radiation: selective impairment of the nitric oxide component of endothelium-dependent vasodilation.

    Soloviev, Anatoly I / Tishkin, Sergey M / Parshikov, Alexander V / Ivanova, Irina V / Goncharov, Eugene V / Gurney, Alison M

    British journal of pharmacology

    2003  Volume 138, Issue 5, Page(s) 837–844

    Abstract: 1) Gamma radiation impairs vascular function, leading to the depression of endothelium-dependent vasodilatation. Loss of the nitric oxide (NO) pathway has been implicated, but little is known about radiation effects on other endothelial mediators. (2) ... ...

    Abstract (1) Gamma radiation impairs vascular function, leading to the depression of endothelium-dependent vasodilatation. Loss of the nitric oxide (NO) pathway has been implicated, but little is known about radiation effects on other endothelial mediators. (2) This study investigated the mechanisms of endothelial dysfunction in rabbits subjected to whole-body irradiation from a cobalt(60) source. (3) The endothelium-dependent relaxation of rabbit aorta evoked by acetylcholine (ACh) or A23187 was impaired in a dose-dependent manner by irradiation at 2 Gy or above. Inhibition was evident 9 days post-irradiation and persisted over the 30 day experimental period. (4) Endothelium-independent responses to glyceryl trinitrate (GTN), sodium nitroprusside (SNP) and 3-morpholino-sydnonimine (SIN-1) were suppressed over a similar dose range at 7-9 days post-irradiation, but recovered fully by 30 days post-irradiation. (5) In healthy vessels, ACh-induced relaxation was inhibited by L-N(omega)-nitroarginine (L-NA; 3 x 10(-4) M) and charybdotoxin (10(-8) M) plus apamin (10(-6) M) but resistant to indomethacin, indicating the involvement of NO and endothelium-derived hyperpolarizing factor (EDHF). Supporting this, ACh caused smooth muscle hyperpolarization that was reduced by L-NA and charybdotoxin plus apamin. (6) In irradiated vessels, responses to ACh were insensitive to L-NA but abolished by charybdotoxin plus apamin, indicating selective loss of NO-mediated relaxation. (7) In animals treated shortly after irradiation with the antioxidant, alpha-tocopherol acetate, the NO-dependent relaxation was restored without effect on the EDHF-dependent component. (8) The results imply that radiation selectively impairs the NO pathway as a consequence of oxidative stress, while EDHF is able to maintain endothelium-dependent relaxation at a reduced level.
    MeSH term(s) Animals ; Aorta, Thoracic/drug effects ; Aorta, Thoracic/physiology ; Aorta, Thoracic/radiation effects ; Dose-Response Relationship, Drug ; Dose-Response Relationship, Radiation ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/physiology ; Endothelium, Vascular/radiation effects ; In Vitro Techniques ; Male ; Nitric Oxide/physiology ; Nitric Oxide/radiation effects ; Rabbits ; Radiation, Ionizing ; Vasodilation/drug effects ; Vasodilation/physiology ; Vasodilation/radiation effects
    Chemical Substances Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2003-03-14
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80081-8
    ISSN 1476-5381 ; 0007-1188
    ISSN (online) 1476-5381
    ISSN 0007-1188
    DOI 10.1038/sj.bjp.0705079
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