Role of bradykinin-NO pathway in prevention of cardiac hypertrophy by ACE inhibitor in rat cardiomyocytes

Ishigai, Yutaka; Mori, Toshio; Ikeda, Toshiko; Fukuzawa, Akiko; Shibano, Toshiro

doi:10.1152/ajpheart.1997.273.6.h2659

Cited by 49 publications

(46 citation statements)

References 20 publications

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“…Moreover, the serum levels of these inhibitors after administration of 8 mg/kg to rats were similar to those found in clinical practice. 13,14,27,28 The inhibitors were started 1 or 4 weeks after the pig serum treatment, which models the typical clinical situation better than the administration of the inhibitors at onset of fibrogenesis induction. Furthermore, these inhibitors were effective not only in the pig serum-induced model but also in fibrosis induced by a choline-deficient amino acid diet (data not shown).…”

Section: Discussionmentioning

confidence: 99%

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Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats

et al. 2001

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The renin-angiotensin system (RAS) is frequently activated in patients with chronic liver diseases. Angiotensin-II (AT-II) has been suggested to play an important role in liver fibrogenesis. It induces hepatic stellate cell (HSC) proliferation and up-regulates the transforming growth factor ␤ 1 (TGF-␤ 1 ) expression via AT-II type 1 receptor (AT 1 -R) in vitro. The aim of the present study was to examine the in vivo effect of candesartan (CA), a clinically used AT 1 -R blocker (ARB), and perindopril (PE), an angiotensin-converting enzyme (ACE) inhibitor (ACE-I), on pig serum-induced liver fibrosis development in rats. The clinically available comparable doses of CA and PE significantly attenuated the fibrosis development. These inhibitory effects of PE and CA were also found in the on-going liver fibrosis model. The hepatic hydroxyproline and serum fibrosis markers were significantly suppressed by CA and PE treatment. Furthermore, the ␣ smooth muscle actin (␣-SMA) positive cells in number were markedly suppressed by CA and PE treatment. Similarly, the hepatic TGF-␤ 1 protein and messenger RNA (mRNA) levels were significantly suppressed. Our in vitro study showed that AT-II increased the TGF-␤ 1 mRNA expression in the activated HSCs, and this effect was totally blocked by CA. These results suggested that the RAS, especially AT-II and AT 1 -R interaction plays a pivotal role in liver fibrosis development through HSC activation. Because both CA and PE are widely used in clinical practice without serious side effects, these drugs may provide an effective new strategy for anti-liver fibrosis therapy. (HEPATOLOGY 2001; 34:745-750.)

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Section: Discussionmentioning

confidence: 99%

“…13,14 We also examined the effect of PE and CA on the on-going fibrosis model. Four weeks after the pig serum injection, the animals in G4 and G5 started to receive PE and CA in the same way as G2 and G3.…”

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Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats

et al. 2001

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“…The D and I alleles are usually associated with higher and lower ACE enzyme activity respectively (Danser et al 1995;Tiret et al 1992;Williams et al 2005). The primary role of ACE in the renin-angiotensin system is to convert angiotensin I into angiotensin II (Rigat et al 1990), which not only acts as a vasoconstrictor but also regulates smooth (Berk et al 1989;Geisterfer et al 1988) and cardiac muscle growth (Sadoshima et al 1993;Ishigai et al 1997). ACE inhibitors have been shown to inhibit hypertrophy in overloaded muscle, which also suggests a role for angiotensin II in skeletal muscle hypertrophy (Gordon et al 2001;Westerkamp and Gordon 2005).…”

Section: Genotype-phenotype Association Studiesmentioning

confidence: 99%

Genes and the ageing muscle: a review on genetic association studies

Garatachea

Lucía

2011

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Western populations are living longer. Ageing decline in muscle mass and strength (i.e. sarcopenia) is becoming a growing public health problem, as it contributes to the decreased capacity for independent living. It is thus important to determine those genetic factors that interact with ageing and thus modulate functional capacity and skeletal muscle phenotypes in older people. It would be also clinically relevant to identify 'unfavourable' genotypes associated with accelerated sarcopenia. In this review, we summarized published information on the potential associations between some genetic polymorphisms and muscle phenotypes in older people. A special emphasis was placed on those candidate polymorphisms that have been more extensively studied, i.e. angiotensinconverting enzyme (ACE) gene I/D, α-actinin-3 (ACTN3) R577X, and myostatin (MSTN) K153R, among others. Although previous heritability studies have indicated that there is an important genetic contribution to individual variability in muscle phenotypes among old people, published data on specific gene variants are controversial. The ACTN3 R577X polymorphism could influence muscle function in old women, yet there is controversy with regards to which allele (R or X) might play a 'favourable' role. Though more research is needed, up-to-date MSTN genotype is possibly the strongest candidate to explain variance among muscle phenotypes in the elderly. Future studies should take into account the association between muscle phenotypes in this population and complex gene-gene and gene-environment interactions.

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“…Several recent reports suggest that activation of the B2-kinin receptors (B2R) could reduce the proliferative effect of several growth factors in cultured cell lines (15,45,50) and in mesangial cells (1,18). B2-kinin receptor is involved in the antihypertrophic effect of BK documented in cultured cardiomyocytes (30,52,53,55) but also in vivo, mainly in the heart (24,25,40,56). Moreover, the antihypertrophic effect of BK in vivo on the renal vasculature in mice has been also reported (67).…”

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ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

Allard¹,

Buléon²,

Cellier³

et al. 2007

American Journal of Physiology-Renal Physiology

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Tack I, Girolami J-P. ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats. Am J Physiol Renal Physiol 293: F1083-F1092, 2007. First published June 27, 2007; doi:10.1152/ajprenal.00401.2006 is associated with increased oxidative stress, overexpression and activation of growth factor receptors, including those for transforming growth factor-␤1 (TGF-␤-RII), platelet-derived growth factor (PDGF-R), and insulin-like growth factor (IGF1-R). These pathways are believed to represent pathophysiological determinants of DN. Beyond perfect glycemic control, angiotensin-converting enzyme inhibitors (ACEI) are the most efficient treatment to delay glomerulosclerosis. Since their mechanisms of action remain uncertain, we investigated the effect of ACEI on the glomerular expression of these growth factor pathways in a model of streptozotocin-induced diabetes in rats. The early phase of diabetes was found to be associated with an increase in glomerular expression of IGF1-R, PDGF-R, and TGF-␤-RII and activation of IRS1, Erk 1/2, and Smad 2/3. These changes were significantly reduced by ACEI treatment. Furthermore, ACEI stimulated glutathione peroxidase activity, suggesting a protective role against oxidative stress. ACEI decreased ANG II production but also increased bradykinin bioavailability by reducing its degradation. Thus the involvement of the bradykinin pathway was investigated using coadministration of HOE-140, a highly specific nonpeptidic B2-kinin receptor antagonist. Almost all the previously described effects of ACEI were abolished by HOE-140, as was the increase in glutathione peroxidase activity. Moreover, the well-established ability of ACEI to reduce albuminuria was also prevented by HOE-140. Taken together, these data demonstrate that, in the early phase of diabetes, ACEI reverse glomerular overexpression and activation of some critical growth factor pathways and increase protection against oxidative stress and that these effects involve B2-kinin receptor activation.angiotensin-converting enzyme inhibitor; oxidative stress; glutathione peroxidase activity; diabetes DIABETIC NEPHROPATHY (DN) causes the majority of end-stage renal diseases throughout the world (54). It was initially believed that elevated blood glucose was the major cause of renal damage in both type 1 and 2 diabetes. However, several clinical studies have demonstrated that strict glycemic control is not sufficient to prevent the progression of renal dysfunction and the development of glomerular lesions. The mechanisms underlying the progression of diabetic kidney disease are intricate and still not completely understood. Among the many pathophysiological mechanisms possible, several growth factors and cytokines have been put forward to account for the onset of DN. This is particularly the case for the paracrine expression of insulin-like growth factor-1 (IGF-1), transforming growth factor-␤ (TGF-␤) (20), and platelet-derived growth factor (PDG...

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Role of bradykinin-NO pathway in prevention of cardiac hypertrophy by ACE inhibitor in rat cardiomyocytes

Cited by 49 publications

References 20 publications

Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats

Angiotensin-II type 1 receptor interaction is a major regulator for liver fibrosis development in rats

Genes and the ageing muscle: a review on genetic association studies

ACE inhibitor reduces growth factor receptor expression and signaling but also albuminuria through B2-kinin glomerular receptor activation in diabetic rats

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