EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles

J. C. Falcone, H. Bohlen

Research output: Contribution to journalArticle

78 Citations (Scopus)

Abstract

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 languageEnglish
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume258
Issue number5 27-5
StatePublished - 1990

Fingerprint

Venules
Arterioles
Acetylcholine
Intestines
Dilatation
Skeletal Muscle
Communication
Muscles
Dithiothreitol
Methylene Blue
Tetrodotoxin
Vasodilation
Indomethacin
Adenosine
Prostaglandins
Endothelium
Reflex

Keywords

  • acetylcholine
  • Endothelial-derived relaxing factor

ASJC Scopus subject areas

  • Physiology

Cite this

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title = "EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles",
abstract = "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.",
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T1 - EDRF from rat intestine and skeletal muscle venules causes dilation of arterioles

AU - Falcone, J. C.

AU - Bohlen, H.

PY - 1990

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N2 - 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.

AB - 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.

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