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Mechanism of Reactive Dilation in Soleus Feed Arteries
Author(s) -
Gray Eric,
Carter Matthew R.,
Jasperse Jeffrey L.
Publication year - 2012
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.26.1_supplement.1138.28
Subject(s) - mechanosensitive channels , chemistry , nitric oxide , medicine , anatomy , biophysics , endocrinology , biochemistry , biology , receptor , ion channel
We have previously shown that reactive dilation of isolated resistance arteries is dependent on both magnitude and duration of pressure reduction. We sought to determine the mechanism for these differences. Rat soleus feed arteries (n=54) were isolated, cannulated, and intraluminal pressure was set at either 65 or 115 cmH 2 O. Intraluminal pressure was reduced to 14 cmH 2 O from either baseline pressure for 1 or 2 min and returned abruptly to baseline pressure, causing a temporary dilation lasting 1–2 minutes. Increasing either duration or baseline pressure increased the magnitude of dilation (1m‐65 = 22.9±2, 1m‐115 = 32.2±2.4, 2m‐65 = 29±2.1, 2m‐115 = 45.1±2.8 max % dilation). Inhibition of nitric oxide production (300 μM L‐NNA) or inhibition of mechanosensitive cation channels (50 μM gadolinium) both failed to alter reactive dilation. Likewise, inhibiting depolymerization of actin filaments (100 nM jasplakinolide) did not reduce reactive dilation. Finally, neither inhibition of tyrosine kinase activity (5 μM genistein) nor inhibition of large Ca 2+ activated K + channels (BK Ca ) (5 μM iberiotoxin) reduced reactive dilation. These data indicate that reactive dilation of soleus feed arteries is not dependent on nitric oxide, mechanosensitive cation channels, actin depolymerization, tyrosine‐kinase activity, or BK Ca . The mechanism responsible for reactive dilation of soleus feed arteries remains unknown.