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Acute behavioral stress‐induced circulating endothelin‐1 is derived from the endothelium (857.9)
Author(s) -
Loria Analia,
Johns Robin,
Hyndman Kelly X,
Yanagisawa Masashi,
Pollock Jennifer
Publication year - 2014
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.28.1_supplement.857.9
Subject(s) - endocrinology , medicine , endothelium , endothelin 1 , endothelin receptor , chemistry , norepinephrine , knockout mouse , biology , receptor , dopamine
Acute behavioral stress increases plasma ET‐1 levels. We hypothesize that a source of the stress‐induced ET‐1 is the endothelium. We utilized a unique mouse model of vascular endothelial‐specific ET‐1 knockout (VEETKO) mice. Male VEETKO and flox control mice were exposed to cage switch stress (CSS). No differences in ET receptor expression in lung tissue were found between flox and VEETKO mice, revealing a normal ET‐1 clearance capability in both genotypes. Measurements of plasma ET‐1 levels and tissue prepro‐ET‐1 mRNA were assessed at baseline (BL) or after 30 min of CSS. VEETKO mice had reduced BL plasma ET‐1 levels compared with flox mice (p<0.05), as previously reported. At BL, pre‐proET‐1 mRNA levels were lower in aorta and renal vessels (p<0.05) in VEETKO mice compared to flox control, but no differences were found in renal or adrenal tissues. Flox control mice displayed a CSS‐induced rise in plasma ET‐1 (p<0.05), however CSS did not induce an elevation in plasma ET‐1 in VEETKO mice. Plasma norepinephrine (NE) was not different between flox and VEETKO mice either at BL or CSS. In response to CSS, there was a reduction in adrenal tissue NE content in both VEETKO and flox mice (p<0.05). We conclude that endothelium‐derived ET‐1 is an important mechanism by which acute behavioral stress increases cardiovascular reactivity. Grant Funding Source : PO1 HL 69999