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Increased arterial pressure response to angiotensin II in mice with mutation in the Lysosomal Trafficking Regulator gene
Author(s) -
beyer andreas Meredith,
Morgan Donald,
Anderson Michael G,
Rahmouni Kamal
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.814.2
Subject(s) - medicine , endocrinology , angiotensin ii , oxidative stress , blood pressure , regulator , mean arterial pressure , endothelial dysfunction , chemistry , knockout mouse , renin–angiotensin system , gene , heart rate , biochemistry , receptor
Exfoliation syndrome (XFS) is commonly associated with disturbance in elasticity, oxidative stress and increased risk for aortic aneurism. Mice carrying a mutation in the lysosomal trafficking regulator ( Lyst ) gene recapitulate many of the phenotypes of human XFS. Therefore, these mice are used to understand the pathophysiological mechanisms of XFS. We previously showed that Lyst mice have endothelial dysfunction. Here, we tested whether the vascular defects alter arterial pressure in these mice. For this, we used radiotelemetry to examine the arterial pressure (AP) of Lyst mice , which are on a C57BL/6J genetic background, as compared to C57BL/6J control mice, at baseline (during 6 days) and in response to a slow acting dose of angiotensin II (ANG II, 600 ng/kg/h, sc) for 14 days. At baseline, Lyst mice exhibited lower heart rate (528±17 vs. 584±7 bpm, P<0.05) and increased daytime mean AP (109±3 vs. 104±1 mmHg). ANG II caused a significant increase in mean AP in C57/BL6J mice (23±2 mmHg). Interestingly, ANG II‐induced mean AP increase was significantly enhance in Lyst mice (36±4 mmHg, P<0.05 vs. controls). These data indicates that endothelial dysfunction found in the Lyst mice is associated with higher baseline AP and increased response to ANG II.