What does this research mean for the field?

Acute exposure to supraphysiological glucose levels enhances noradrenaline sensitivity and impairs endothelium-dependent relaxation in rat mesenteric resistance arteries through mechanisms involving abnormal cyclo-oxygenase activity, reduced nitric oxide release, increased free radical production, and polyol pathway activation. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

The aim is to evaluate how hyperglycaemia affects the function of isolated rat mesenteric resistance arteries.

November 1, 1994British Journal of PharmacologyOpen Access

The effect of hyperglycaemia on function of rat isolated mesenteric resistance artery

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Why the study?

Does exposure to supraphysiological glucose alter noradrenaline sensitivity and acetylcholine-induced relaxation in isolated rat mesenteric resistance arteries?

Population

Mesenteric resistance arteries from female Wistar rats (220-250 g)

Comparison

Isotonic supraphysiological glucose solutions vs Physiological buffer

Design

Preclinical

Follow-up

2 h incubation

Authors

PTPaul TaylorKing's College London LPLucilla PostonUniversity of Southern California

Discussion

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Implication

Caution against clinical extrapolation from rat vessels; leaves open hyperglycemia mechanisms in human resistance arteries.

Key Points

The aim is to evaluate how hyperglycaemia affects the function of isolated rat mesenteric resistance arteries.
Isolated mesenteric arteries from female Wistar rats were incubated in glucose solutions (20 and 45 mM) for 2 hours.
Noradrenaline sensitivity and acetylcholine-induced relaxation were assessed after incubation.
Pharmacological interventions were applied to dissect the underlying mechanisms.
Arteries in 20 mM glucose showed increased noradrenaline sensitivity compared to controls. Effect on acetylcholine-induced relaxation was impaired in both glucose concentrations.
Indomethacin normalized sensitivity to noradrenaline in 20 mM glucose but revealed enhanced responsiveness in high glucose.
Addition of L-arginine and ponalrestat improved relaxation responses in high glucose, suggesting roles for nitric oxide synthesis and the polyol pathway.

Structured PICO

Does exposure to supraphysiological glucose alter noradrenaline sensitivity and acetylcholine-induced relaxation in isolated rat mesenteric resistance arteries?

Population

Mesenteric resistance arteries from female Wistar rats (220-250 g)

Intervention

Isotonic supraphysiological glucose solutions (20 and 45 mM, in physiological buffer, 2 h incubation)

Comparator

Physiological buffer

Outcome

Noradrenaline sensitivity and acetylcholine-induced relaxationsurrogate

Hyperglycemia impairs endothelium-dependent relaxation and enhances noradrenaline sensitivity in rat mesenteric arteries, likely mediated by abnormal cyclo-oxygenase activity, reduced nitric oxide, free radicals, and polyol pathway activation.

Cite This Study

Taylor et al. (1994) studied this question.

synapsesocial.com/papers/6a1bf89700ee29383e9d3d5c https://doi.org/10.1111/j.1476-5381.1994.tb17064.x

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The effect of hyperglycaemia on function of rat isolated mesenteric resistance artery

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

The effect of hyperglycaemia on function of rat isolated mesenteric resistance artery

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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