Premium
Flow‐dependent regulation of arteriolar diameter in rat skeletal muscle in situ: role of endothelium‐derived relaxing factor and prostanoids.
Author(s) -
Friebel M,
Klotz K F,
Ley K,
Gaehtgens P,
Pries A R
Publication year - 1995
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.1995.sp020616
Subject(s) - chemistry , skeletal muscle , endothelium , biophysics , flow (mathematics) , anatomy , medicine , biology , mechanics , physics
1. Arteriolar diameter in the resting rat spinotrapezius muscle was studied by intravital video microscopy before and after blockade of the L‐arginine‐EDRF (NG‐nitro‐L‐arginine, L‐NNA) or the cyclo‐oxygenase‐prostacyclin (indomethacin) pathway. Blockade of either pathway leads to a decrease of arteriolar diameter of 25‐40%, while the combined blockade of both results in vasoconstriction of 50‐60%. 2. Alteration of blood flow velocity elicited by partial micropipette occlusion induces corresponding changes of vessel diameter. The flow‐dependent diameter response is reduced by about 80% by L‐NNA. By contrast, blockade of prostanoid production shows no significant influence on vessel response to blood flow alteration in the range tested. 3. Transient overshooting vasodilatation is seen for about 1 min following the sudden restoration of flow velocity subsequent to occlusion. In contrast to the initial phase of this response, the late phase is blocked by L‐NNA. 4. The findings suggest that basal release of endothelium‐derived relaxing factor (EDRF) and prostanoids leads to additive and independent dilator effects, and that flow‐dependent diameter changes are primarily mediated by EDRF. 5. If present data are compared with literature reports, it appears that arterial flow sensitivity is most pronounced in the smallest vessels. In such vessels, flow‐dependent dilatation will amplify even small changes of volume flow by more than four times.