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Flow-dependent increase of ICAM-1 on saphenous vein endothelium is sensitive to apamin

Department of Vascular Surgery, Imperial College at Charing Cross, London W6 8RP, United Kingdom

Submitted 7 October 2003 ; accepted in final form 9 February 2004

The potassium channel blocker tetraethylammonium blocks the flow-induced increase in endothelial ICAM-1. We have investigated the subtype of potassium channel that modulates flow-induced increased expression of ICAM-1 on saphenous vein endothelium. Cultured human saphenous vein endothelial cells (HSVECs) or intact saphenous veins were perfused at fixed low and high flows in a laminar shear chamber or flow rig, respectively, in the presence or absence of potassium channel blockers. Expression of K⁺ channels and endothelial ICAM-1 was measured by real-time polymerase chain reaction and/or immunoassays. In HSVECs, the application of 0.8 N/m² (8 dyn/cm²) shear stress resulted in a two- to fourfold increase in cellular ICAM-1 within 6 h (P < 0.001). In intact vein a similar shear stress, with pulsatile arterial pressure, resulted in a twofold increase in endothelial ICAM-1/CD31 staining area within 1.5 h (P < 0.001). Both increases in ICAM-1 were blocked by inclusion of 100 nM apamin in the vein perfusate, whereas other K⁺ channel blockers were less effective. Two subtypes of small conductance Ca²⁺-activated K⁺ channel (selectively blocked by apamin) were expressed in HSVECs and vein endothelium (SK3>SK2). Apamin blocked the upregulation of ICAM-1 on saphenous vein endothelium in response to increased flow to implicate small conductance Ca²⁺-activated K⁺ channels in shear stress/flow-mediated signaling pathways.

cardiovascular surgery; endothelial function; hemodynamics; K⁺ channel

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