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Flow Conditions Affect Metabolic Vasodilation in Mouse Cremaster Arterioles
Author(s) -
Best Derek Douglas,
Sarelius Ingrid H.
Publication year - 2006
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.20.4.a270-c
Subject(s) - vasodilation , cremaster muscle , glibenclamide , contraction (grammar) , microcirculation , dilation (metric space) , arteriole , chemistry , medicine , anatomy , endocrinology , cardiology , geometry , mathematics , diabetes mellitus
We sought to determine if the NO, K ATP channel , and H 2 O 2 dependent components of the metabolic dilation are sensitive to flow. In the cremaster muscle of anesthetized mice (74 mg/kg ip), electrical field stimulation of the cremaster muscle (15 sec, 30 Hz, 0.2 msec, 5‐10 V) was used to produce a metabolic vasodilation. Free flow conditions produced a dilation of 17.7 ± 1.4 μm from a baseline of 7.1 ± 2.4 μm (max diameter 28.7 ± 2.3 μm, n=6). This response was not attenuated by 100 μM Nitro‐L‐arginine (LNA); 17.8 ± 1.7 μm (max diameter 28.4 ± 1.8 μm, n=6). Blocking K ATP channels with 10 μM glibenclamide did not attenuate the peak dilation; 19.3 ± 1.6 μm (max diameter 30.3 ± 1.8 μm, n=6), but did dramatically decrease the recovery time. Muscle contraction in normoxic ischemic tissues produced a dilation of 11.3 ± 2.5 μm in control vessels, which was significantly less than the dilation in free flow (n=13, P < 0.001). With 100 μM LNA, the peak dilation was, again, not affected, (10.8 ± 2.8 μm from a baseline of 3.9 ± 0.6 μm, n= 5). With 10 μM glibenclamide, the dilation was significantly attenuated from free flow dilation (4.0 ± 1.4 μm, n=7 from a baseline of 3.9 ± 0.5 μm, P < 0.001, n=7). We conclude that metabolic vasodilation is sensitive to flow in a manner that implicates K ATP channel but not NO dependent pathways. Catalase (500 units/ml, 1.3 ± 0.2 μm from a baseline of 13.4 ± 1.1 μm, n=5) attenuates metabolic vasodilation in ischemic arterioles but also decreased resting arteriole tone to 9.9 ± 1.0 μm from a baseline of 3.5 ± 0.5 μm, n=5. Thus, H 2 O 2 dependent signaling may also be involved in metabolic vasodilation. (Supported by NIH HL 76414)