What does this research mean for the field?

The obesity-related impairment in acetylcholine-mediated endothelium-dependent vasodilation in the human forearm is not caused by reduced muscarinic receptor responsiveness or sensitivity. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To determine whether impaired acetylcholine-mediated vasodilator response in obese adults is caused by reduced muscarinic receptor responsiveness or sensitivity.

February 1, 2006Journal of Cardiovascular Pharmacology

Impaired Endothelium-Dependent Vasodilation in Normotensive and Normoglycemic Obese Adult Humans

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Why the study?

Does obesity impair acetylcholine-mediated vasodilation due to reduced muscarinic receptor responsiveness in normotensive and normoglycemic adults?

Population

28 sedentary middle-aged normotensive and normoglycemic adults, including 14 normal weight and 14 obese…

Comparison

Intraarterial infusion of acetylcholine and… vs Normal weight adults

Design

Cross-sectional

Authors

GGGary P. Van GuilderWestern Colorado University GHGreta L. HoetzerWilmington University DDDonald R. DengelUniversity of Minnesota

Discussion

Member takes

Implication

Obesity-linked impairment in acetylcholine vasodilation is unrelated to muscarinic sensitivity; leaves open alternative endothelial mechanisms for study.

Key Points

To determine whether impaired acetylcholine-mediated vasodilator response in obese adults is caused by reduced muscarinic receptor responsiveness or sensitivity.
Studied 28 sedentary middle-aged adults: 14 normal weight (BMI 23.6 ± 0.5 kg/m²) and 14 obese (BMI 32.2 ± 0.9 kg/m²).
Measured forearm blood flow via intra-arterial infusion of acetylcholine (8–128 µg/min) and sodium nitroprusside (2.0–8.0 µg/min).
Forearm blood flow responses to acetylcholine were 25% lower in obese adults (4.2 ± 0.3 to 12.0 ± 0.8 mL/100 mL tissue/min) versus normal-weight adults (4.4 ± 0.3 to 16.9 ± 1.0 mL/100 mL tissue/min; P < 0.01).
EC50 for acetylcholine-induced vasodilation was not different between obese (7.8 ± 0.8 µg/min) and normal-weight (7.8 ± 0.6 µg/min) adults, with flow plateauing above 32 µg/min in both cohorts.
Vasodilator responses to sodium nitroprusside showed no significant differences between the two groups.

Structured PICO

Does obesity impair acetylcholine-mediated vasodilation due to reduced muscarinic receptor responsiveness in normotensive and normoglycemic adults?

Population

28 sedentary middle-aged normotensive and normoglycemic adults, including 14 normal weight and 14 obese individuals

Intervention

Intraarterial infusion of acetylcholine (8-128 microg/min) and sodium nitroprusside (2.0-8.0 microg/min)

Comparator

Normal weight adults

Outcome

Forearm blood flow (FBF) response to intraarterial infusion of acetylcholine and sodium nitroprussidesurrogate

The impairment of endothelium-dependent vasodilation in obese adults is not caused by reduced muscarinic receptor responsiveness or sensitivity.

Cite This Study

Guilder et al. (2006) studied this question.

synapsesocial.com/papers/6a1e7c09c07483b92c55efea https://doi.org/10.1097/01.fjc.0000205097.29946.d3

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Implication

Obesity-linked impairment in acetylcholine vasodilation is unrelated to muscarinic sensitivity; leaves open alternative endothelial mechanisms for study.

Impaired Endothelium-Dependent Vasodilation in Normotensive and Normoglycemic Obese Adult Humans

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Impaired Endothelium-Dependent Vasodilation in Normotensive and Normoglycemic Obese Adult Humans

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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