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Smith ELK et al.  
Vascular endothelial growth factor (VEGF)and endothelin-3 (ET-3) activate cation currents in human umbilical vein endothelial cells

Journal of Clinical and Basic Cardiology 1998; 1 (1): 52-54

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Fig. 1: VEGV und ET-3 - Gefäßpermeabilität Fig. 2: VEGF und ET-3 - Gefäßpermeabilität Fig. 3: VEGF und ET-3 - Gefäßpermeabilität

Keywords: Elektrophysiologieendothelinvaskulärer Permeabilitätsfaktorelectrophysiologyendothelinvascular permeability factor

Proliferation of endothelial cells is an essential process in repair following vascular injury and also in angiogenesis and vasculogenesis. Factors that influence endothelial proliferation are thus of great clinical and pharmacological interest. The endogenous peptides vascular endothelial growth factor (VEGF) and endothelin-3 (ET-3, acting via ETB receptor activation) both potently stimulate regrowth of human umbilical vein endothelial cells (HUVEC) following mechanical wounding in vitro. The aim of this study was to test for electrophysiological correlates of these trophic effects. In single HUVEC, whole cell currents were activated within 10 min after exposure to either VEGF (20 pmol/L) or ET-3 (100 nmol/L) the reversal voltage being -59 mV in each case. Either VEGF or ET-3 induced currents in cells at the edge of a wound in more than half the cells studied. However, ETB receptor agonist sarafatoxin S6c (40 nmol/L) did not. Thus the ET-3-induced currents are likely to be the result of ETA receptor stimulation. ET-3 induced no current in cells distant from a regrowing boundary. These observations are consistent with a single population of cation channels that are activated by either peptide and are weakly selective for potassium ions (pK/pNa = 3). The observed currents are probably not directly involved in the growth promoting effects of ET-3 and VEGF. J Clin Basic Cardiol 1998; 1: 52-4.
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