Communication from venules to arterioles through the release of endothelial-derived relaxing factor (EDRF) was evaluated. To demonstrate that the rat intestinal and the spinotrapezius muscle arterioles can respond to EDRF, the vessels were dilated by iontophoretically applied acetylcholine (ACh), and this dilation was greatly attenuated by the inhibitors of EDRF actions, methylene blue (100 μM) and dithiothreitol (50 μM). The EDRF inhibitors did not suppress arteriolar dilation to topically applied adenosine (10-4 M), an endothelium-independent dilator. Although ACh release onto the venular wall had minimal effects on the diameter of the venule, the paired arteriole would dilate 20-30% in the intestine and 50-60% in the spinotrapezius muscle. After EDRF inhibition, venular ACh exposure did not cause arteriolar dilation. ACh diffusion from venules to arterioles was not the cause of arteriolar dilation, because release of ACh into the tissue at the same distance as from the arteriole to the venular ACh release site caused minimal arteriolar dilation. Neither blockade of neural reflexes with tetrodotoxin (3 x 10-6 M) nor suppression of prostaglandin formation with indomethacin (10-5 M) prevented the arteriolar dilation during release of ACh onto the venular wall. The overall study indicated that communication from venules to arterioles through the release of EDRF from the venule did occur and caused substantial arteriolar vasodilation. Therefore circumstances within and around venules may influence regulation of nearby arterioles through an EDRF-mediated mechanism.
|Original language||English (US)|
|Journal||American Journal of Physiology - Heart and Circulatory Physiology|
|Issue number||5 27-5|
|State||Published - Jan 1 1990|
- Endothelial-derived relaxing factor
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