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March 15, 1995The Journal of PhysiologyOpen Access

Blockade of either pathway decreased arteriolar diameter by 25-40%, combined blockade by 50-60%; flow-dependent diameter response was reduced by about 80% by L-NNA but not significantly by indomethacin.

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Population

Rat spinotrapezius muscle in situ

Comparison

Blockade of the L-arginine-EDRF pathway or the… vs Baseline (before blockade)

Design

Preclinical

Authors

MFM.F. FriebelKKK.‐F. KlotzKLKlaus Ley

Discussion

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Overview

Animal data on EDRF-prostanoid arteriolar control should not change practice; leaves open human translation of flow-mediated mechanisms.

Structured PICO

P
Population
Rat spinotrapezius muscle in situ
I
Intervention
Blockade of the L-arginine-EDRF pathway (NG-nitro-L-arginine, L-NNA) or the cyclo-oxygenase-prostacyclin pathway (indomethacin), and alteration of blood flow velocity via partial micropipette occlusion
C
Comparator
Baseline (before blockade)
O
Outcome
Arteriolar diameter changessurrogate

Basal release of EDRF and prostanoids have additive and independent dilator effects, while flow-dependent diameter changes are primarily mediated by EDRF in rat skeletal muscle arterioles.

Cite This Study

Friebel et al. (1995) studied this question.

synapsesocial.com/papers/6a7f381c290a50e19e6f399chttps://doi.org/10.1113/jphysiol.1995.sp020616
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