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Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide.

Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Research Abstract Details 

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  • Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Abstract Text:

    william j perkinsWilliam J Perkins,miwa taniguchiMiwa Taniguchi,david o warnerDavid O Warner,eduardo n chiniEduardo N Chini,keith a jonesKeith A Jones,

    In a newly characterized cultured porcine pulmonary artery (PA) preparation, 24-h treatment with the nitric oxide (NO) donor (Z)-1-[N-(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate (DETA-NO) decreased the response to acutely applied DETA-NO compared with 24-h control (-log EC(50) 6.55 +/- 0.12 and 5.02 +/- 0.21, respectively). Treatment of PA with the cell-permeable superoxide dismutase mimetic, Mn(III) tetra(4-benzoic acid) porphyrin chloride, did not change NO responsiveness in either freshly prepared or 24-h DETA-NO-treated PA. cGMP and cAMP phosphodiesterase activities were approximately equal in PA. Twenty-four-hour DETA-NO treatment did not change either cGMP or cAMP phosphodiesterase activities. Twenty-four hours in culture had no significant effect on soluble guanylyl cyclase (sGC) subunit mRNA expression, but 24-h DETA-NO treatment significantly decreased the expression of both sGCalpha(1) and sGCbeta(1). sGCbeta(1) protein expression was 42 +/- 4 ng/mg soluble protein. Twenty-four hours in culture without and with DETA-NO reduced sGCbeta(1) protein expression (36 +/- 3 and 31 +/- 3 ng/mg soluble protein, respectively, P < 0.025). Basal tissue cGMP [(cGMP)(i)] was significantly increased, and NO-induced (cGMP)(i) was significantly decreased by 24-h DETA-NO treatment. (cGMP)(i) normalized to the amount of sGC protein expressed in PA was significantly lower in PA treated for 24 h with DETA-NO compared with both freshly isolated and 24-h cultured PA. We conclude that prolonged NO treatment induces decreased acute NO responsiveness in part by decreasing both sGC expression and sGC-specific activity.

    Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Publishing Authors By Initials

    wj perkinsWJ Perkins,m taniguchiM Taniguchi,do warnerDO Warner,en chiniEN Chini,ka jonesKA Jones,

    For similar organic chemicals: triazenes research abstracts see: organic chemicals: triazenes research

    PUBMED ID PMID:

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    Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Journal Published:

    PUBLICATION TYPE: Research Support, N.I.H., Extr

    Journal: American journal of physiology. Lung cellular and

    VOLUME: 293

    Page Numbers: L84-95

    Journal Abbreviation: Am. J. Physiol. Lung Cell Mol.

    ISSN: 1040-0605

    DAY: 23

    MONTH: 03

    YEAR: 2007

    Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Information

    Number of References:

    LANGUAGE: eng

    NlmUniqueID: 100901229

    Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Keywords Mesh Terms:

    KEYWORDS: Triazenes

    MESH TERMS: pharmacology

    Chemical & Substance for Abstract: Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide. Information

    Substance Name: soluble guanylyl cyclase

    Registry Number: EC 4.6.1.2

    Grant and Affiliation Information for Reduction in soluble guanylyl cyclase-specific activity following prolonged treatment of porcine pulmonary artery with nitric oxide.

    AFFILIATION: Department of Anesthesiology, Mayo Clinic College of Medicine, 200 First St. SW, Rochester, MN 55905, USA. perkinsw@mayo.edu

    Country: United States

    United States Research PublicationUnited States Research Publication

    AGENCY: United States NHLBI

    GRANT: HL-69968

    ACRONYM: HL

    MEDLINETA: Am J Physiol Lung Cell Mol Phy

    REFSOURCE:

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