September 1, 2002AJP Heart and Circulatory Physiology

EDHF, but not NO or prostaglandins, is critical to evoke a conducted dilation upon ACh in hamster arterioles

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Population

Hamster cremaster microcirculation arterioles

Comparison

Local stimulation with acetylcholine or sodium… vs Responses without specific blockers, or SNP…

Design

Preclinical

Authors

BHBernd HoepflUniversity of Lübeck BRBarbara RodenwaldtUniversity of Lübeck UPUlrich PohlCentre of Experimental Medicine of the Slovak Academy of Sciences

Discussion

Member takes

Implication

P-450-dependent EDHF mediates conducted dilation in hamster arterioles; leaves open relevance to human vessels or therapy.

Structured PICO

Population

Hamster cremaster microcirculation arterioles

Intervention

Local stimulation with acetylcholine (ACh) or sodium nitroprusside (SNP), with or without blockade of NO synthase, cyclooxygenase, P-450 monooxygenase (sulfaphenazole, 17-octadecynoic acid), or Ca(2+)-dependent K(+) channels (charybdotoxin, iberiotoxin)

Comparator

Responses without specific blockers, or SNP compared to ACh

Outcome

Changes in arteriolar diameter at the site of application and up to 1.4 mm upstreamsurrogate

In hamster arterioles, endothelium-derived hyperpolarizing factor (EDHF) generated via cytochrome P-450 monooxygenase, rather than NO or prostaglandins, is the critical mediator initiating conducted vasodilation upon acetylcholine stimulation.

Cite This Study

Hoepfl et al. (2002) studied this question.

synapsesocial.com/papers/6a866b0785b962098c2fdad5 https://doi.org/10.1152/ajpheart.01082.2001

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EDHF, but not NO or prostaglandins, is critical to evoke a conducted dilation upon ACh in hamster arterioles

Discussion

Member takes

Implication

Structured PICO

Cite This Study

EDHF, but not NO or prostaglandins, is critical to evoke a conducted dilation upon ACh in hamster arterioles

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider