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- Sanjay Rajagopalan
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Jørn Bech Laursen
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Alain Borthayre
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Sabine Kurz
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Joan Keiser
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Steven Haleen
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- Adel Giaid
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
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- David G. Harrison
- From the Department of Medicine, Division of Cardiology, Emory University School of Medicine (S.R., J.B.L., A.B., S.K., D.G.H.), Atlanta, Ga; the Atlanta (Ga) Veterans Administration Medical Center (D.G.H.); Department of Pathology, McGill University, Montreal, Canada (J.B.L., A.G.); Rigshospital, Copenhagen, Denmark (J.B.L.); and Parke-Davis Pharmaceutical Research, Ann Arbor, Mich (J.K., S.H.).
この論文をさがす
説明
<jats:p><jats:italic>Abstract</jats:italic>Experiments in cultured vascular smooth muscle cells have shown that angiotensin II (Ang II) stimulates expression of endothelin-1. We sought to examine role of endothelin-1 in the effects of Ang II in vivo. Ang II infusion in rats (0.7 mg/kg per day for 5 days) was associated with marked increases in vascular smooth muscle endothelin-1 levels, as assessed by immunostaining. Administration of the selective endothelin type A (ET<jats:sub>A</jats:sub>) receptor antagonist PD 155080 (50 mg/kg per day) abrogated the hypertensive response to a 5-day infusion of Ang II (0.7 mg/kg per day), as did losartan (25 mg/kg per day). ET<jats:sub>A</jats:sub>receptor blockade during Ang II–mediated hypertension was associated with marked elevations of plasma endothelin-1 levels. Ang II–mediated hypertension was associated with heightened vascular responsiveness to a variety of vasoconstrictor agents except endothelin-1. Blockade of ET<jats:sub>A</jats:sub>receptor invariably corrected this vasoconstrictor hyperresponsiveness. We conclude that some of the vascular effects of Ang II thought to be unique to this hormone are likely mediated by endothelin-1.</jats:p>
収録刊行物
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- Hypertension
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Hypertension 30 (1), 29-34, 1997-07
Ovid Technologies (Wolters Kluwer Health)
