Endogenous angiotensin II suppresses insulin signaling in vascular smooth muscle cells from spontaneously hypertensive rats

Fukuda, Noboru; Satoh, Chikara; Hu, Wen Yang; Nakayama, Mikiyasu; Kishioka, Hirobumi; Kanmatsuse, Katsuo

doi:10.1097/00004872-200109000-00018

Cited by 46 publications

(37 citation statements)

References 20 publications

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“…This suggests that normal growth of intestinal muscularis is regulated by other IRS-1-linked hormones than IGF-I, which could include growth hormone and angiotensin II, which both have trophic effects on smooth muscle and both activate IRS-1 (6,17).…”

Section: Discussionmentioning

confidence: 99%

Cell-specific effects of insulin receptor substrate-1 deficiency on normal and IGF-I-mediated colon growth

Simmons¹,

Ling²,

Wilkins³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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Section: Discussionmentioning

confidence: 99%

Cell-specific effects of insulin receptor substrate-1 deficiency on normal and IGF-I-mediated colon growth

Simmons¹,

Ling²,

Wilkins³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…Ang II has been found to attenuate or inhibit insulin signalling in vascular smooth muscle cells (Vellosa et al 1996, Folli et al 1997, Fukuda et al 2001, implicating a role for the RAS in regulating the actions of insulin. Recent experiments have shown that Ang II is a potent inducer of renal oxidative stress, both in vivo and in vitro (Hannken et al 1998, James et al 1998, Haugen et al 2000.…”

Section: Discussionmentioning

confidence: 99%

Reactive oxygen species blockade and action of insulin on expression of angiotensinogen gene in proximal tubular cells

Hsieh¹,

Fustier²,

Wei³

et al. 2004

Journal of Endocrinology

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We reported previously that insulin inhibits the stimulatory effect of high glucose on the expression of angiotensinogen (ANG) gene in both rat immortalized renal proximal tubular cells (IRPTCs) and non-diabetic rat renal proximal tubular cells (RPTCs), but has no effect in diabetic rat RPTCs. In the present study we investigated whether hyperglycaemia-induced resistance to the insulininduced inhibition of expression of the ANG gene is mediated via the generation of reactive oxygen species (ROS) in RPTCs. Rat IRPTCs were cultured for 2 weeks in high-glucose (25 mM) or normal-glucose (5 mM) medium plus angiotensin II (Ang II) with or without a superoxide scavenger (tiron), or inhibitors of: NADPH oxidase (diphenylene iodinium, DPI), Ang II type 1 and 2 receptors (losartan and PD123319), angiotensinconverting enzyme (perindopril), protein kinase C (GF 109203X), or glutamine:fructose-6-phosphate aminotransferase (azaserine). Cellular generation of ROS, and ANG and renin mRNA levels were assessed by lucigenin assay and specific reverse transcriptase-PCR respectively. Phosphorylation of p44/42 mitogen-activated protein kinase (p44/42 MAPK) was evaluated by western blotting. Prolonged exposure of IRPTCs to high concentrations of glucose or Ang II evoked generation of ROS and resistance to the insulin-induced inhibition of expression of the ANG gene and of p44/42 MAPK phosphorylation. Co-incubation of IRPTCs with tiron, DPI, losartan, PD123319, perindopril, GF 109203X or azaserine prevented ROS generation, restoring the inhibitory action of insulin on ANG gene expression and on p44/42 MAPK phosphorylation. In conclusion, our studies demonstrate that blockade of both ROS generation and activation of the intrarenal renin-angiotensin system improves the inhibitory action of insulin on ANG gene expression in IRPTCs in conditions of high glucose.

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“…The overactivity of the RAS is likely to impair insulin signaling and contribute to the insulin resistance observed in essential hypertension [7]. Accordingly, the activation of the RAS was shown to modulate muscle insulin signaling, leading to a decrease in insulin-stimulated glucose uptake [45,46]. At the molecular level, captopril improves insulin action by increasing IRS-1 tyrosine phosphorylation and association with PI 3-kinase [39].…”

Section: The Cross-talk At the Extracellular Levelmentioning

confidence: 99%

The multi‐faceted cross‐talk between the insulin and angiotensin II signaling systems

Velloso

Folli

Perego

et al. 2006

Diabetes Metabolism Res

103

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SummaryInsulin and angiotensin II are hormones that play pivotal roles in the control of two vital and closely related systems, the metabolic and the circulatory systems, respectively. A failure in the proper action of each of these hormones results, to a variable degree, in the development of two highly prevalent and commonly overlapping diseases -diabetes mellitus and hypertension. In recent years, a series of studies has revealed a tight connection between the signal transduction pathways that mediate insulin and angiotensin II actions in target tissues. This molecular cross-talk occurs at multiple levels and plays an important role in phenomena that range from the action of anti-hypertensive drugs to cardiac hypertrophy and energy acquisition by the heart. At the extracellular level, the angiotensin-converting enzyme controls angiotensin II synthesis but also interferes with insulin signaling through the proper regulation of angiotensin II and through the accumulation of bradykinin. At an early intracellular level, angiotensin II, acting through JAK-2/IRS-1/PI3-kinase, JNK and ERK, may induce the serine phosphorylation and inhibition of key elements of the insulin-signaling pathway. Finally, by inducing the expression of the regulatory protein SOCS-3, angiotensin II may impose a late control on the insulin signal. This review will focus on the main advances obtained in this field and will discuss the implications of this molecular cross-talk in the common clinical association between diabetes mellitus and hypertension.

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Endogenous angiotensin II suppresses insulin signaling in vascular smooth muscle cells from spontaneously hypertensive rats

Abstract: These results indicate that endogenous Ang II suppresses insulin signaling in VSMC from SHR by activating extracellular signal-regulated kinase. These findings suggest that tissue Ang II may play a role in insulin resistance in hypertension.

Cited by 46 publications

References 20 publications

Cell-specific effects of insulin receptor substrate-1 deficiency on normal and IGF-I-mediated colon growth

Cell-specific effects of insulin receptor substrate-1 deficiency on normal and IGF-I-mediated colon growth

Reactive oxygen species blockade and action of insulin on expression of angiotensinogen gene in proximal tubular cells

The multi‐faceted cross‐talk between the insulin and angiotensin II signaling systems

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