Angiotensin II Receptor Subtypes in the Skeletal Muscle Vasculature of Patients With Severe Congestive Heart Failure

Malendowicz, S.; Ennezat, Pierre Vladimir; Testa, Marco; Murray, Laura E.; Sonnenblick, Edmund H.; Evans, Todd; LeJemtel, Thierry H.

doi:10.1161/01.cir.102.18.2210

Cited by 32 publications

(16 citation statements)

References 26 publications

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“…ACE and AT1 mRNA expressions have also been detected in the skeletal muscle of patients with chronic heart failure [24,25]. Ang II has been considered to be related to cardiac and cancer cachexia [26,27] by activating ubiquitin-proteasome proteolytic pathway [28].…”

Section: Discussionmentioning

confidence: 99%

Intramuscular renin–angiotensin system is activated in human muscular dystrophy

Sun¹,

Haginoya²,

Dai³

et al. 2009

Journal of the Neurological Sciences

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Section: Discussionmentioning

confidence: 99%

Intramuscular renin–angiotensin system is activated in human muscular dystrophy

Sun¹,

Haginoya²,

Dai³

et al. 2009

Journal of the Neurological Sciences

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“…Although improvements in blood flow to skeletal muscles may mediate some of the improvements in glucose uptake with AT1 receptor (AT 1 R) blockade, there is mounting evidence that ANG II, acting via the AT 1 R, inhibits insulin signaling and glucose transport (5,8,24). ANG II is synthesized by skeletal muscle tissue (24,54), and AT 1 R are plentiful in skeletal muscle (32,36). Indeed, skeletal muscle comprises Ͼ40% of mammalian body mass (21) and is the major site of insulinstimulated glucose disposal (6).…”

mentioning

confidence: 99%

Abrogation of oxidative stress improves insulin sensitivity in the Ren-2 rat model of tissue angiotensin II overexpression

Blendea¹,

Jacobs²,

Stump³

et al. 2005

American Journal of Physiology-Endocrinology and Metabolism

155

154

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To evaluate the role of renin-angiotensin system (RAS)-mediated oxidative stress in insulin resistance (IR), we compared the effects of the angiotensin II (ANG II) receptor blocker (ARB) valsartan and a superoxide dismutase (SOD) mimetic, tempol, on whole body glucose tolerance and soleus muscle insulin-stimulated glucose uptake in transgenic hypertensive TG(mREN-2)27 (Ren-2) rats. Ren-2 rats and Sprague-Dawley (SD) controls were given valsartan (30 mg/kg) or tempol (1 mmol/l) in their drinking water for 21 days. IR was measured by glucose tolerance testing (1 g/kg glucose ip). IR index (AUC(glucose) x AUC(insulin)) was significantly higher in the Ren-2 animals compared with SD controls (30.5 +/- 7.0 x 10(6) arbitrary units in Ren-2 vs. 10.2 +/- 2.4 x 10(6) in SD, P < 0.01). Both valsartan and tempol treatment normalized Ren-2 IR index. Compared with SD controls (100%), there was a significant increase in superoxide anion production (measured by lucigenin-enhanced chemiluminescence) in soleus muscles of Ren-2 rats (133 +/- 15%). However, superoxide production was reduced in both valsartan- and tempol-treated (85 +/- 22% and 59 +/- 12%, respectively) Ren-2 rats. Insulin (INS)-mediated 2-deoxyglucose (2-DG) uptake (%SD basal levels) was substantially lower in Ren-2 rat soleus muscle compared with SD (Ren-2 + INS = 110 +/- 3% vs. SD + INS = 206 +/- 12%, P < 0.05). However, Ren-2 rats treated with valsartan or tempol exhibited a significant increase in insulin-mediated 2-DG uptake compared with untreated transgenic animals. Improvements in skeletal muscle insulin-dependent glucose uptake and whole body IR in rats overexpressing ANG II by ARB or SOD mimetic indicate that oxidative stress plays an important role in ANG II-mediated insulin resistance.

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“…However, published evidence confirms only the presence of the AT1 receptor in human skeletal muscle. Transcripts from the AT2 receptor gene are not detected in adult muscles, suggesting that ACE inhibition is unlikely to inhibit any possible benefit of AT2 receptor stimulation [27] .…”

Section: Renin-angiotensin Systemmentioning

confidence: 99%

Sarcopenia – A Potential Target for Angiotensin-Converting Enzyme Inhibition?

Sumukadas

Struthers²,

McMurdo³

2006

Gerontology

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Society is ageing. There has been a steady increase in the number of people aged 65 years and over throughout the 20th century and this trend is predicted to continue worldwide. This has resulted in an increase in the incidence of sarcopenia, which is a loss of muscle mass and function with age. Maintenance of muscular function into old age is critical to sustaining normal daily activity and functional independence. Sarcopenia is associated with increased morbidity and mortality. Till now most efforts to counteract sarcopenia have met with limited success. We postulate that targeting the renin-angiotensin system through angiotensin-converting enzyme (ACE) inhibition could play a role in countering sarcopenia. ACE inhibitors could work by preventing mitochondrial decline and improving endothelial function and muscle metabolism. We describe the literature to support our hypothesis that sarcopenia may be a potential therapeutic target for ACE inhibitors.

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Angiotensin II Receptor Subtypes in the Skeletal Muscle Vasculature of Patients With Severe Congestive Heart Failure

Abstract: The AT2-R gene is not expressed in the skeletal muscle of patients with CHF. In the absence of detectable AT2-R gene transcripts, the AT2-R pathway is unlikely to contribute to the effects of AT1-R antagonists on the skeletal muscle vasculature in patients with severe CHF.

Cited by 32 publications

References 26 publications

Intramuscular renin–angiotensin system is activated in human muscular dystrophy

Intramuscular renin–angiotensin system is activated in human muscular dystrophy

Abrogation of oxidative stress improves insulin sensitivity in the Ren-2 rat model of tissue angiotensin II overexpression

Sarcopenia – A Potential Target for Angiotensin-Converting Enzyme Inhibition?

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