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Time‐dependency of angiotensin II mediated vasomotor dysfunction
Author(s) -
Erkuran Yilmaz Cigdem,
Granger D. Neil
Publication year - 2009
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.23.1_supplement.774.3
Subject(s) - vasomotor , angiotensin ii , endothelium , medicine , vasodilation , endocrinology , renin–angiotensin system , acetylcholine , endothelial dysfunction , blood pressure
Angiotensin II (AngII), the main effector of the renin‐angiotensin system, plays an essential role in the regulation of blood pressure and it has been implicated in the pathogenesis of cardiovascular diseases. While AngII is known to alter endothelial function, the time‐course of this response remains poorly understood. The aim of this study was to compare the effects of acute vs chronic angiotensin II treatment on endothelium‐dependent vasomotor function. Wire myography was used to assess vasomotor function of aortic rings obtained from C57BL/6J male mice. Aortic rings were incubated with angiotensin II for either either 15 minutes or 4 hours. In another group, aortic rings were isolated from WT mice subjected to chronic AngII infusion (Alzet pump) at a rate of 2000 ng/kg/min for 14 days. Endothelium‐dependent vasomotor function was assessed by monitoring acetylcholine‐induced vasorelaxation. While AngII exposure for 15 min did not alter endothelium‐dependent vasomotor function, 4 h incubation with AngII significantly (~50%) impaired endothelium dependent vasodilation, compared to untreated rings. A similar level of vasomotor impairment was noted in aortic rings from mice subjected to chronic AngII infusion. These findings reveal a time‐dependency of AngII mediated vasomotor dysfunction and indicates that this response occurs via a mechanism that likely involves new protein synthesis. (HL26441)