Angiotensin II Stimulates Intercellular Adhesion Molecule-1 (ICAM-1) Expression by Human Vascular Endothelial Cells and Increases Soluble ICAM-1 Release In Vivo
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- L. Pastore
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- A. Tessitore
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- S. Martinotti
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- E. Toniato
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- E. Alesse
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- M. C. Bravi
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- C. Ferri
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- G. Desideri
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- A. Gulino
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
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- A. Santucci
- From the University of L’Aquila, Departments of Experimental (L.P., A.T., S.M., E.T., E.A.) and Internal Medicine (M.C.B., G.D., A.S.), and the University La Sapienza, I Clinica Medica–Andrea Cesalpino Foundation (C.F.) and Department of Experimental Medicine (A.G.), Rome; and the Neuromed Institute, Pozzilli (A.G.), Italy.
抄録
<jats:p> <jats:italic>Background</jats:italic> —We evaluated whether angiotensin II (Ang II) influenced intercellular adhesion molecule (ICAM)-1 expression by human vascular endothelial cells derived from umbilical cord veins (HUVECs) and plasma soluble ICAM-1 levels in vivo. </jats:p> <jats:p> <jats:italic>Methods and Results</jats:italic> —Cultured HUVECs were incubated with Ang II (from 10 <jats:sup>−9</jats:sup> to 10 <jats:sup>−6</jats:sup> mol/L) with or without candesartan and PD12319 (inhibitors of Ang II AT <jats:sub>1</jats:sub> and AT <jats:sub>2</jats:sub> receptors, respectively) for various times up to 4 hours. Total RNA was then extracted from HUVECs, and Northern blots were probed with a 1.9-kb ICAM-1 cDNA fragment. HUVEC supernatants were used to assess soluble ICAM-1 release by ELISA. Northern blot analysis detected a strong increase of ICAM-1 mRNA after 2-hour incubation with Ang II. The response was inhibited by candesartan. Soluble ICAM-1 release by HUVECs also increased ( <jats:italic>P</jats:italic> <0.002) after 2-hour Ang II stimulation. In vivo, Ang II (at an initial rate of 1.0 ng · kg <jats:sup>−1</jats:sup> · min <jats:sup>−1</jats:sup> , to be increased each 30 minutes by 2.0 ng · kg <jats:sup>−1</jats:sup> · min <jats:sup>−1</jats:sup> to the final rate of 7.0 ng · kg <jats:sup>−1</jats:sup> · min <jats:sup>−1</jats:sup> ) was infused in 8 normotensive and 12 essential hypertensive individuals. In the latter, Ang II was reinfused after 4 weeks on either placebo (n=3), losartan (50 mg UID, n=5), or atenolol (50 mg UID, n=4) treatment. Plasma soluble ICAM-1 levels increased after Ang II infusion in hypertensives and normotensives ( <jats:italic>P</jats:italic> <0.0001 after 90 minutes). Losartan reduced baseline soluble ICAM-1 levels ( <jats:italic>P</jats:italic> <0.05) and Ang II–related ICAM-1 increments. </jats:p> <jats:p> <jats:italic>Conclusions</jats:italic> —Ang II upregulates ICAM-1 expression by HUVECs and stimulates in vitro and in vivo soluble ICAM-1 release. AT <jats:sub>1</jats:sub> receptor blockade inhibits such endothelial effects of Ang II. </jats:p>
収録刊行物
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- Circulation
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Circulation 100 (15), 1646-1652, 1999-10-12
Ovid Technologies (Wolters Kluwer Health)
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詳細情報 詳細情報について
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- CRID
- 1362544420084396416
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- ISSN
- 15244539
- 00097322
- http://id.crossref.org/issn/00097322
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- データソース種別
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- Crossref