What does this research mean for the field?

Insulin resistance, rather than hyperinsulinemia alone, leads to enhanced vascular contractile responses mediated by altered voltage-dependent calcium channel function, which may contribute to the pathogenesis of hypertension in insulin resistance syndrome. Novelty: ClaimNovelty.INCREMENTAL. Consensus alignment: ConsensusAlignment.NEUTRAL.

What question did this study set out to answer?

To evaluate how chronic hyperinsulinemia and insulin resistance alter vascular smooth muscle contractile tension and intracellular free calcium dynamics in response to vasoactive stimuli.

July 1, 1996Diabetes

Augmented Contractile Function and Abnormal Ca2+ Handling in the Aorta of Zucker Obese Rats With Insulin Resistance

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Population

Male Wistar rats (n=20) and Zucker obese/lean rats. Aortic smooth muscle preparations without endothelium.

Comparison

Continuous subcutaneous infusion of insulin (18… vs Vehicle infusion (Wistar rats); Zucker lean rats.

Design

Preclinical

Follow-up

2 weeks

Authors

YOYasuyoshi OuchiGeneral / Preventive / Lipids SHShu-zhong HanThe University of Tokyo SKSeungbum KimKorea University

Discussion

Member takes

Implication

Supports altered Ca2+ channel function in insulin resistance-related hypertension; hypothesis-generating for human translation.

Key Points

To evaluate how chronic hyperinsulinemia and insulin resistance alter vascular smooth muscle contractile tension and intracellular free calcium dynamics in response to vasoactive stimuli.
Measured contractile tension and intracellular free calcium simultaneously in fura-2-loaded, endothelium-denuded aortic strips from male Wistar rats receiving continuous insulin infusion (18 nmol/kg/day, n=10) or vehicle (n=10) for 2 weeks.
Assessed aortic strip responses to potassium chloride, phenylephrine, and serotonin in insulin-resistant Zucker obese rats versus Zucker lean controls.
Examined the effect of pre-treatment with the calcium channel agonist Bay K8644 on potassium chloride-induced responses in both lean and obese rats.
Insulin-infused rats attained plasma insulin levels of 930 ± 54 pmol/L but exhibited decreased calcium and tension responses to potassium chloride and phenylephrine compared with vehicle controls.
Zucker obese rats displayed markedly enhanced tension and calcium responses to potassium chloride, phenylephrine, and serotonin compared with Zucker lean controls.
Bay K8644 pre-treatment increased potassium chloride-stimulated responses in lean rat aortas to levels matching obese rats, but produced no additional response in obese rat aortas.

Structured PICO

Population

Male Wistar rats (n=20) and Zucker obese/lean rats. Aortic smooth muscle preparations without endothelium.

Intervention

Continuous subcutaneous infusion of insulin (18 nmol x kg(-1) x day(-1)) for 2 weeks (Wistar rats); genetic insulin resistance (Zucker obese rats). Exposure to vasoactive substances (KCl, phenylephrine, serotonin, Bay K8644).

Comparator

Vehicle infusion (Wistar rats); Zucker lean rats.

Outcome

Tension and intracellular free calcium concentration ([Ca2+]i) of aortic smooth musclesurrogate

Enhanced vascular contractile responses in insulin resistance may be due to altered voltage-dependent Ca2+ channel function, contributing to the pathogenesis of hypertension.

Cite This Study

Ouchi et al. (1996) studied this question.

synapsesocial.com/papers/6a19b9061d4d911c80ea8a60 https://doi.org/10.2337/diab.45.3.s55

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Augmented Contractile Function and Abnormal Ca2+ Handling in the Aorta of Zucker Obese Rats With Insulin Resistance

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

Augmented Contractile Function and Abnormal Ca2+ Handling in the Aorta of Zucker Obese Rats With Insulin Resistance

Discussion

Member takes

Implication

Key Points

Structured PICO

Cite This Study

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