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(Circulation. 1999;100:1646-1652.)
© 1999 American Heart Association, Inc.
Basic Science Reports |
Angiotensin II Stimulates Intercellular Adhesion Molecule-1 (ICAM-1) Expression by Human Vascular Endothelial Cells and Increases Soluble ICAM-1 Release In Vivo
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.
Correspondence to Claudio Ferri, MD, Università La Sapienza, I Clinica Medica, 00161 Roma, Italy. E-mail clferri{at}axrma.uniroma1.it
Background—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.
Methods and Results—Cultured HUVECs were incubated with Ang II (from 10-9 to 10-6 mol/L) with or without candesartan and PD12319 (inhibitors of Ang II AT1 and AT2 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 (P<0.002) after 2-hour Ang II stimulation. In vivo, Ang II (at an initial rate of 1.0 ng · kg-1 · min-1, to be increased each 30 minutes by 2.0 ng · kg-1 · min-1 to the final rate of 7.0 ng · kg-1 · min-1) 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 (P<0.0001 after 90 minutes). Losartan reduced baseline soluble ICAM-1 levels (P<0.05) and Ang II–related ICAM-1 increments.
Conclusions—Ang II upregulates ICAM-1 expression by HUVECs and stimulates in vitro and in vivo soluble ICAM-1 release. AT1 receptor blockade inhibits such endothelial effects of Ang II.
Key Words: cell adhesion molecules • endothelium • cells • angiotensin
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