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Functional response to endothelin in macro‐ and microvascular endothelial cells
Author(s) -
Shlyonsky Vadim,
Ben Soussia Ismail,
Cheriaa Nidhal,
Naeije Robert,
Mies Frederique
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.976.8
Subject(s) - endothelin 1 , endothelin receptor , endothelial stem cell , endothelins , intracellular , endocrinology , chemistry , calcium in biology , receptor , medicine , microcirculation , biophysics , microbiology and biotechnology , biology , in vitro , biochemistry
Several studies suggest that macro‐ and microvascular endothelial cells differ in their structure and function. We compared human pulmonary microvascular endothelial cells (MvEC) with human macrovascular endothelial cells from pulmonary artery (PAEC) and from aorta (AoEC) with regard to their functional response to endothelin‐1. We used RTQ‐PCR, whole‐cell patch‐clamp technique, Fluo‐4 measurements of intracellular calcium and NO‐release measurements in order to study functional effect of endothelin‐1. RNA expression of endothelin receptor B was detected in AoEC, PAEC and MvEC. Expression of ETB receptor in MvEC was 3–5 times higher compared to AoEC and PAEC. Endothelin‐1 transiently increased membrane permeability of all three types of endothelial cells. There was no difference in peak ion current response between these different cells, however integral response (duration and current increase) of MvEC was bigger compared to PAEC and AoEC. By the contrast, measurements of intracellular calcium increase by endothelin‐1 did not reveal any difference in this functional response between cells tested. Finally, NO‐release in response to endothelin‐1 was not detectable in PAEC and AoEC, while in MvEC endotheline‐1 stimulated significant NO‐production. These results suggest, that microvascular endothelial cells present more pronounced ability to respond to endothelin‐1, thus balancing its vasoconstrictive action in microvasculature. Supported by FNRS and ULB funds .