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Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling

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Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling. / Mollnau, Hanke; Wendt, Maria; Szöcs, Katalin; Lassègue, Bernard; Schulz, Eberhard; Oelze, Mathias; Li, Huige; Bodenschatz, Martin; August, Michael; Kleschyov, Andrei L; Tsilimingas, Nikolaus; Walter, Ulrich; Förstermann, Ulrich; Meinertz, Thomas; Griendling, Kathy; Münzel, Thomas.

In: CIRC RES, Vol. 90, No. 4, 08.03.2002, p. 58-65.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Mollnau, H, Wendt, M, Szöcs, K, Lassègue, B, Schulz, E, Oelze, M, Li, H, Bodenschatz, M, August, M, Kleschyov, AL, Tsilimingas, N, Walter, U, Förstermann, U, Meinertz, T, Griendling, K & Münzel, T 2002, 'Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling', CIRC RES, vol. 90, no. 4, pp. 58-65. https://doi.org/10.1161/01.res.0000012569.55432.02

APA

Mollnau, H., Wendt, M., Szöcs, K., Lassègue, B., Schulz, E., Oelze, M., Li, H., Bodenschatz, M., August, M., Kleschyov, A. L., Tsilimingas, N., Walter, U., Förstermann, U., Meinertz, T., Griendling, K., & Münzel, T. (2002). Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling. CIRC RES, 90(4), 58-65. https://doi.org/10.1161/01.res.0000012569.55432.02

Vancouver

Mollnau H, Wendt M, Szöcs K, Lassègue B, Schulz E, Oelze M et al. Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling. CIRC RES. 2002 Mar 8;90(4):58-65. https://doi.org/10.1161/01.res.0000012569.55432.02

Bibtex

@article{7ee7aa75bd0a438baa9674d45216e453,
title = "Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling",
abstract = "Angiotensin II infusion causes endothelial dysfunction by increasing NAD(P)H oxidase-mediated vascular superoxide production. However, it remains to be elucidated how in vivo angiotensin II treatment may alter the expression of the gp91(phox) isoforms and the endothelial nitric oxide synthase (NOS III) and subsequent signaling events and whether, in addition to the NAD(P)H oxidase, NOS III contributes to vascular superoxide formation. We therefore studied the influence of in vivo angiotensin II treatment (7 days) in rats on endothelial function and on the expression of the NAD(P)H oxidase subunits p22(phox), nox1, nox4, and gp91(phox) and NOS III. Further analysis included the expression of NO-downstream targets, the soluble guanylyl cyclase (sGC), the cGMP-dependent protein kinase I (cGK-I), and the expression and phosphorylation of the vasodilator-stimulated phosphoprotein (VASP) at Ser239 (P-VASP). Angiotensin II caused endothelial dysfunction and increased vascular superoxide. Likewise, we found an increase in vascular protein kinase C (PKC) activity, in the expression of nox1 (6- to 7-fold), gp91(phox) (3-fold), p22(phox) (3-fold), NOS III mRNA, and protein. NOS-inhibition with N(G)-nitro-L-arginine decreased superoxide in vessels from angiotensin II-treated animals, compatible with NOS-uncoupling. Vascular NO assessed with electron paramagnetic resonance was markedly reduced. Likewise, a decrease in sGC-expression and P-VASP levels was found. In vivo PKC-inhibition with chelerythrine reduced angiotensin II-induced superoxide production and markedly inhibited upregulation of NAD(P)H oxidase subunits. We therefore conclude that angiotensin II-induced increases in the activity and the expression of NAD(P)H oxidase are at least in part PKC-dependent. NADPH oxidase-induced superoxide production may trigger NOS III uncoupling, leading to impaired NO/cGMP signaling and to endothelial dysfunction in this animal model. The full text of this article is available at http://www.circresaha.org.",
keywords = "Angiotensin II/administration & dosage, Animals, Aorta/metabolism, Blood Pressure/drug effects, Cell Adhesion Molecules/metabolism, Cyclic GMP/metabolism, Cyclic GMP-Dependent Protein Kinase Type I, Cyclic GMP-Dependent Protein Kinases/metabolism, Disease Models, Animal, Enzyme Activation/drug effects, Guanylate Cyclase, In Vitro Techniques, Infusions, Parenteral, Membrane Glycoproteins/genetics, Membrane Transport Proteins, Microfilament Proteins, NAD/pharmacology, NADH, NADPH Oxidoreductases/genetics, NADP/pharmacology, NADPH Dehydrogenase/genetics, NADPH Oxidase 1, NADPH Oxidase 2, NADPH Oxidase 4, NADPH Oxidases/genetics, Nitric Oxide/metabolism, Nitric Oxide Synthase/genetics, Nitric Oxide Synthase Type III, Phosphoproteins/genetics, Protein Kinase C/metabolism, Rats, Rats, Wistar, Receptors, Cytoplasmic and Nuclear/metabolism, Signal Transduction/drug effects, Soluble Guanylyl Cyclase, Superoxides/metabolism, Vasodilation/drug effects, Vasodilator Agents/pharmacology",
author = "Hanke Mollnau and Maria Wendt and Katalin Sz{\"o}cs and Bernard Lass{\`e}gue and Eberhard Schulz and Mathias Oelze and Huige Li and Martin Bodenschatz and Michael August and Kleschyov, {Andrei L} and Nikolaus Tsilimingas and Ulrich Walter and Ulrich F{\"o}rstermann and Thomas Meinertz and Kathy Griendling and Thomas M{\"u}nzel",
year = "2002",
month = mar,
day = "8",
doi = "10.1161/01.res.0000012569.55432.02",
language = "English",
volume = "90",
pages = "58--65",
journal = "CIRC RES",
issn = "0009-7330",
publisher = "Lippincott Williams and Wilkins",
number = "4",

}

RIS

TY - JOUR

T1 - Effects of angiotensin II infusion on the expression and function of NAD(P)H oxidase and components of nitric oxide/cGMP signaling

AU - Mollnau, Hanke

AU - Wendt, Maria

AU - Szöcs, Katalin

AU - Lassègue, Bernard

AU - Schulz, Eberhard

AU - Oelze, Mathias

AU - Li, Huige

AU - Bodenschatz, Martin

AU - August, Michael

AU - Kleschyov, Andrei L

AU - Tsilimingas, Nikolaus

AU - Walter, Ulrich

AU - Förstermann, Ulrich

AU - Meinertz, Thomas

AU - Griendling, Kathy

AU - Münzel, Thomas

PY - 2002/3/8

Y1 - 2002/3/8

N2 - Angiotensin II infusion causes endothelial dysfunction by increasing NAD(P)H oxidase-mediated vascular superoxide production. However, it remains to be elucidated how in vivo angiotensin II treatment may alter the expression of the gp91(phox) isoforms and the endothelial nitric oxide synthase (NOS III) and subsequent signaling events and whether, in addition to the NAD(P)H oxidase, NOS III contributes to vascular superoxide formation. We therefore studied the influence of in vivo angiotensin II treatment (7 days) in rats on endothelial function and on the expression of the NAD(P)H oxidase subunits p22(phox), nox1, nox4, and gp91(phox) and NOS III. Further analysis included the expression of NO-downstream targets, the soluble guanylyl cyclase (sGC), the cGMP-dependent protein kinase I (cGK-I), and the expression and phosphorylation of the vasodilator-stimulated phosphoprotein (VASP) at Ser239 (P-VASP). Angiotensin II caused endothelial dysfunction and increased vascular superoxide. Likewise, we found an increase in vascular protein kinase C (PKC) activity, in the expression of nox1 (6- to 7-fold), gp91(phox) (3-fold), p22(phox) (3-fold), NOS III mRNA, and protein. NOS-inhibition with N(G)-nitro-L-arginine decreased superoxide in vessels from angiotensin II-treated animals, compatible with NOS-uncoupling. Vascular NO assessed with electron paramagnetic resonance was markedly reduced. Likewise, a decrease in sGC-expression and P-VASP levels was found. In vivo PKC-inhibition with chelerythrine reduced angiotensin II-induced superoxide production and markedly inhibited upregulation of NAD(P)H oxidase subunits. We therefore conclude that angiotensin II-induced increases in the activity and the expression of NAD(P)H oxidase are at least in part PKC-dependent. NADPH oxidase-induced superoxide production may trigger NOS III uncoupling, leading to impaired NO/cGMP signaling and to endothelial dysfunction in this animal model. The full text of this article is available at http://www.circresaha.org.

AB - Angiotensin II infusion causes endothelial dysfunction by increasing NAD(P)H oxidase-mediated vascular superoxide production. However, it remains to be elucidated how in vivo angiotensin II treatment may alter the expression of the gp91(phox) isoforms and the endothelial nitric oxide synthase (NOS III) and subsequent signaling events and whether, in addition to the NAD(P)H oxidase, NOS III contributes to vascular superoxide formation. We therefore studied the influence of in vivo angiotensin II treatment (7 days) in rats on endothelial function and on the expression of the NAD(P)H oxidase subunits p22(phox), nox1, nox4, and gp91(phox) and NOS III. Further analysis included the expression of NO-downstream targets, the soluble guanylyl cyclase (sGC), the cGMP-dependent protein kinase I (cGK-I), and the expression and phosphorylation of the vasodilator-stimulated phosphoprotein (VASP) at Ser239 (P-VASP). Angiotensin II caused endothelial dysfunction and increased vascular superoxide. Likewise, we found an increase in vascular protein kinase C (PKC) activity, in the expression of nox1 (6- to 7-fold), gp91(phox) (3-fold), p22(phox) (3-fold), NOS III mRNA, and protein. NOS-inhibition with N(G)-nitro-L-arginine decreased superoxide in vessels from angiotensin II-treated animals, compatible with NOS-uncoupling. Vascular NO assessed with electron paramagnetic resonance was markedly reduced. Likewise, a decrease in sGC-expression and P-VASP levels was found. In vivo PKC-inhibition with chelerythrine reduced angiotensin II-induced superoxide production and markedly inhibited upregulation of NAD(P)H oxidase subunits. We therefore conclude that angiotensin II-induced increases in the activity and the expression of NAD(P)H oxidase are at least in part PKC-dependent. NADPH oxidase-induced superoxide production may trigger NOS III uncoupling, leading to impaired NO/cGMP signaling and to endothelial dysfunction in this animal model. The full text of this article is available at http://www.circresaha.org.

KW - Angiotensin II/administration & dosage

KW - Animals

KW - Aorta/metabolism

KW - Blood Pressure/drug effects

KW - Cell Adhesion Molecules/metabolism

KW - Cyclic GMP/metabolism

KW - Cyclic GMP-Dependent Protein Kinase Type I

KW - Cyclic GMP-Dependent Protein Kinases/metabolism

KW - Disease Models, Animal

KW - Enzyme Activation/drug effects

KW - Guanylate Cyclase

KW - In Vitro Techniques

KW - Infusions, Parenteral

KW - Membrane Glycoproteins/genetics

KW - Membrane Transport Proteins

KW - Microfilament Proteins

KW - NAD/pharmacology

KW - NADH, NADPH Oxidoreductases/genetics

KW - NADP/pharmacology

KW - NADPH Dehydrogenase/genetics

KW - NADPH Oxidase 1

KW - NADPH Oxidase 2

KW - NADPH Oxidase 4

KW - NADPH Oxidases/genetics

KW - Nitric Oxide/metabolism

KW - Nitric Oxide Synthase/genetics

KW - Nitric Oxide Synthase Type III

KW - Phosphoproteins/genetics

KW - Protein Kinase C/metabolism

KW - Rats

KW - Rats, Wistar

KW - Receptors, Cytoplasmic and Nuclear/metabolism

KW - Signal Transduction/drug effects

KW - Soluble Guanylyl Cyclase

KW - Superoxides/metabolism

KW - Vasodilation/drug effects

KW - Vasodilator Agents/pharmacology

U2 - 10.1161/01.res.0000012569.55432.02

DO - 10.1161/01.res.0000012569.55432.02

M3 - SCORING: Journal article

C2 - 11884382

VL - 90

SP - 58

EP - 65

JO - CIRC RES

JF - CIRC RES

SN - 0009-7330

IS - 4

ER -