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March 1, 2000AJP Heart and Circulatory Physiology

In eNOS knockout mice skeletal muscle arteriolar dilation to acetylcholine is mediated by EDHF

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Population

Isolated, cannulated, and pressurized arterioles of gracilis muscle from male eNOS-KO and wild-type (WT) mice

Comparison

Acetylcholine (10-10 M) with or without inhibitors vs Wild-type (WT) mice arterioles

Design

Preclinical

Authors

AHAn HuangFirst Affiliated Hospital of Jiangxi Medical CollegeDSDong SunShanxi Medical UniversityCSCarolyn J. SmithUniversity of California, Riverside

Discussion

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Implication

Animal evidence of EDHF compensation in eNOS deficiency; leaves open human microvascular relevance.

Structured PICO

P
Population
Isolated, cannulated, and pressurized arterioles of gracilis muscle from male eNOS-KO and wild-type (WT) mice
I
Intervention
Acetylcholine (ACh) (10(-9)-10(-7) M) with or without inhibitors (L-NNA, indomethacin, clotrimazole, miconazole, high K+, iberiotoxin)
C
Comparator
Wild-type (WT) mice arterioles
O
Outcome
Arteriolar dilation response to acetylcholinesurrogate

In the absence of endothelial nitric oxide synthase, endothelium-derived hyperpolarizing factor (EDHF) synthesized via cytochrome P-450 compensates to mediate acetylcholine-induced vasodilation in skeletal muscle arterioles.

Cite This Study

Huang et al. (2000) studied this question.

synapsesocial.com/papers/6a6f7c448031ec7bb1dbc5d3https://doi.org/10.1152/ajpheart.2000.278.3.h762
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Also Consider

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  4. 4Pharmacologic Differentiation Between Endothelium-Dependent Relaxations Sensitive and Resistant to Nitro-L-Arginine in Coronary Arteries1994 · 67 citations
  5. 5Synthesis of lipoxygenase and epoxygenase products of arachidonic acid by normal and stenosed canine coronary arteries.1990 · 110 citations