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Venule‐mediated arteriolar constriction in the NOD mouse retina
Author(s) -
Lee Seungjun,
Harris Norman R
Publication year - 2007
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.21.6.a844-c
Subject(s) - venule , constriction , arteriole , microcirculation , intravital microscopy , endocrinology , losartan , medicine , chemistry , angiotensin ii , anatomy , biology , receptor
Arteriolar constriction (in the rat mesentery) has been reported to occur early in the progression of streptozotocin‐induced diabetes, with the constriction observed in arterioles that are closely paired with postcapillary venules (Microcirculation 11:‐, 2004). Whether a similar pattern of arteriolar constriction is operative in the diabetic retina is unknown, as are the mediators of the venule‐dependent constriction. In this study, non‐obese diabetic (NOD) mice (20–25 g) were used 3 weeks after the onset of hyperglycemia, and the retinas of the anesthetized animals were examined by intravital microscopy. Erythrocytes from donor animals were labeled with a fluorescent dye and injected into the recipients to allow measurement of arteriolar flow rates. Flow rates in closely venule‐paired arterioles in diabetic mice were significantly reduced compared with those of controls, while flow rates of distantly venule‐paired arterioles were not. To investigate the mechanism responsible for the arteriolar constriction, another group of diabetic mice were treated with losartan (angiotensin II receptor antagonist). After losartan treatment, flow tended to increase only in the more closely venule‐paired arterioles. These results support the hypothesis that venule‐derived mediators may be responsible for arteriolar constriction in the diabetic retina, and that angiotensin II may play a role in this mechanism. Supported by JDRF 1‐2003‐159.