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July 6, 2017Experimental PhysiologyOpen Access

TRPV1channels in human skeletal muscle feed arteries: implications for vascular function

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Population

Skeletal muscle feed arteries (SMFAs) from 16 humans (mean age 63 ± 5 years, range 41–89 years)

Comparison

Capsaicin (TRPV1 agonist) vs Control (without capsaicin)

Design

Preclinical

Key result

Capsaicin significantly attenuated maximal vasocontraction in response to phenylephrine (21% vs 52% LTmax) and dexmedetomidine, while enhancing maximal vasorelaxation with ACh.

Authors

SIStephen J. IvesSPSong Young ParkOKOh Sung Kwon

Discussion

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Overview

TRPV1 activation may modulate vascular tone ex vivo; leaves open translation to human cardiovascular outcomes.

Structured PICO

P
Population
16 humans (mean age 63 years, range 41-89) from whom skeletal muscle feed arteries were studied ex vivo.
I
Intervention
Capsaicin (TRPV1 agonist)
C
Comparator
Control (without capsaicin)
O
Outcome
Vascular function (vasocontraction in response to phenylephrine and dexmedetomidine, and vasorelaxation with ACh and sodium nitroprusside)surrogate

Main Result

Absolute Event Rate: 21% vs 52%

Human skeletal muscle feed arteries express functional TRPV1 channels that modulate vascular function by opposing alpha-adrenergic vasocontraction and potentiating endothelium-dependent vasorelaxation.

Cite This Study

Ives et al. (2017) studied this question. Capsaicin vs. Control (without capsaicin) was evaluated on Maximal vasocontraction in response to phenylephrine. Capsaicin significantly attenuated maximal vasocontraction in response to phenylephrine (21% vs 52% LTmax) and dexmedetomidine, while enhancing maximal vasorelaxation with ACh.

synapsesocial.com/papers/6a208d9ec1a20d348eb41a55https://doi.org/10.1113/ep086223
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