Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state
Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constitue...
Ausführliche Beschreibung
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1996 |
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| Umfang: |
9 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Heart failure reviews - 1996, 1(1996) vom: März, Seite 193-201 |
| Übergeordnetes Werk: |
volume:1 ; year:1996 ; month:03 ; pages:193-201 ; extent:9 |
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| 520 | |a Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. | ||
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(DE-627)NLEJ189827610 DE-627 ger DE-627 rakwb eng Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state 1996 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. Springer Online Journal Archives 1860-2002 Balligand, Jean-Luc oth Ungureanu-Longrois, Dan oth Smith, Thomas W. oth in Heart failure reviews 1996 1(1996) vom: März, Seite 193-201 (DE-627)NLEJ188987606 (DE-600)2006431-7 1573-7322 nnns volume:1 year:1996 month:03 pages:193-201 extent:9 http://dx.doi.org/10.1007/BF00127808 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 1 1996 3 193-201 9 |
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(DE-627)NLEJ189827610 DE-627 ger DE-627 rakwb eng Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state 1996 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. Springer Online Journal Archives 1860-2002 Balligand, Jean-Luc oth Ungureanu-Longrois, Dan oth Smith, Thomas W. oth in Heart failure reviews 1996 1(1996) vom: März, Seite 193-201 (DE-627)NLEJ188987606 (DE-600)2006431-7 1573-7322 nnns volume:1 year:1996 month:03 pages:193-201 extent:9 http://dx.doi.org/10.1007/BF00127808 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 1 1996 3 193-201 9 |
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(DE-627)NLEJ189827610 DE-627 ger DE-627 rakwb eng Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state 1996 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. Springer Online Journal Archives 1860-2002 Balligand, Jean-Luc oth Ungureanu-Longrois, Dan oth Smith, Thomas W. oth in Heart failure reviews 1996 1(1996) vom: März, Seite 193-201 (DE-627)NLEJ188987606 (DE-600)2006431-7 1573-7322 nnns volume:1 year:1996 month:03 pages:193-201 extent:9 http://dx.doi.org/10.1007/BF00127808 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 1 1996 3 193-201 9 |
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(DE-627)NLEJ189827610 DE-627 ger DE-627 rakwb eng Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state 1996 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. Springer Online Journal Archives 1860-2002 Balligand, Jean-Luc oth Ungureanu-Longrois, Dan oth Smith, Thomas W. oth in Heart failure reviews 1996 1(1996) vom: März, Seite 193-201 (DE-627)NLEJ188987606 (DE-600)2006431-7 1573-7322 nnns volume:1 year:1996 month:03 pages:193-201 extent:9 http://dx.doi.org/10.1007/BF00127808 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 1 1996 3 193-201 9 |
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(DE-627)NLEJ189827610 DE-627 ger DE-627 rakwb eng Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state 1996 9 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. Springer Online Journal Archives 1860-2002 Balligand, Jean-Luc oth Ungureanu-Longrois, Dan oth Smith, Thomas W. oth in Heart failure reviews 1996 1(1996) vom: März, Seite 193-201 (DE-627)NLEJ188987606 (DE-600)2006431-7 1573-7322 nnns volume:1 year:1996 month:03 pages:193-201 extent:9 http://dx.doi.org/10.1007/BF00127808 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 1 1996 3 193-201 9 |
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Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state |
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Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. |
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Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. |
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Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ189827610</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707132515.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070525s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ189827610</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Role of a cytokine-inducible nitric oxide synthase in the control of myocardial contractile state</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">9</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Nitric oxide (NO) is a nearly ubiquitous intercellular and intracellular chemical messenger produced by a family of enzymes collectively called NO synthases. Evidence from several laboratories documented the expression of the inducible NO synthase, or NOS2, within several cellular constituents of ventricular muscle, including cardiac myocytes, after exposure to inflammatory cytokines in vitro or in vivo. Cardiac microvascular endothelial cells, which are adjacent to myocytes in ventricular myocardium, also express NOS2 in response to cytokines, although NOS2 gene induction is differentially regulated between these two cell types through cell-specific second messenger pathways regulating transcriptional activators. Nitric oxide production in cardiac muscle is also regulated by other post-transcriptional and post-translational mechanisms. The autocrine or paracrine production of NO exerts important inotropic and lusitropic effects on cardiac contraction in several experimental preparations. In most cases, these functional effects are accompanied by NO-dependent increases in intracellular cyclic GMP, which may affect cardiac contraction through regulation of cyclic-AMP generation, L-type calcium current, or myofilament sensitivity to calcium in cardiac myocytes. Other cyclic-GMP-independent actions of NO may also mediate its contractile effects in the heart and may participate in the pathogenesis of the myocardial dysfunction accompanying local or systemic production of cytokines in sepsis, cardiac graft rejection, or heart failure.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Balligand, Jean-Luc</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ungureanu-Longrois, Dan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Smith, Thomas W.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Heart failure reviews</subfield><subfield code="d">1996</subfield><subfield code="g">1(1996) vom: März, Seite 193-201</subfield><subfield code="w">(DE-627)NLEJ188987606</subfield><subfield code="w">(DE-600)2006431-7</subfield><subfield code="x">1573-7322</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:1</subfield><subfield code="g">year:1996</subfield><subfield code="g">month:03</subfield><subfield code="g">pages:193-201</subfield><subfield code="g">extent:9</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00127808</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">1</subfield><subfield code="j">1996</subfield><subfield code="c">3</subfield><subfield code="h">193-201</subfield><subfield code="g">9</subfield></datafield></record></collection>
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