Role of Bradykinin in Renoprotective Effects by Angiotensin II Type 1 Receptor Antagonist in Salt-Sensitive Hypertension.

Yokota, Kazuaki; Kishida, Masayuki; Ogura, Toshio; Suzuki, Jirô; Otsuka, Fumio; Mimura, Yukari; Takeda, Masaya; Nakamura, Yoshio; Makino, Hírofumi

doi:10.1291/hypres.26.265

Cited by 8 publications

(3 citation statements)

References 43 publications

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“…These observations were similar to those in a previous report that showed that cardiac hypertrophy was prevented by ACE inhibitor treatment (14) or angiotensin receptor blockade (19) but not by combining either treatment with BK B2 receptor antagonist.…”

Section: Fig 8 Morphologic Changes Of Rat Coronary Vessels Sectionsupporting

confidence: 92%

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

et al. 2004

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Angiotensin converting enzyme (ACE) inhibitors inhibit both the formation of angiotensin II and the catabolism of bradykinin (BK).sion of angiotensin I into angiotensin II (ATII). ACE inhibitors block not only ATII formation but also bradykinin (BK) degradation. Some pharmacological effects of ACE inhibitors are mediated by endogenous preservation of BK. BK is a potent vasodilator peptide, which possesses cardioprotective action via BK B2 receptor. The binding of BK to B2 receptor activates second messengers that induce a broad spectrum of biological effects, such as vasodilation, inflammation and cell proliferation (5, 6). In cardiovascular systems, BK mediates important effects, including increased vascular permeability, enhanced myocardial glucose uptake,

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Section: Fig 8 Morphologic Changes Of Rat Coronary Vessels Sectionsupporting

confidence: 92%

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

et al. 2004

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“…ACEIs inhibit not only the formation of active ANGII, but also kinin degradation, thereby increasing the level of the potent vasodilator, bradykinin (BK). Despite some conflicting data (Nabokov et al, 1998), evidence is increasing that the renoprotective effects of ACEIs are mediated partly by BK B2 receptor (BK2R) activation (Yokota et al, 2003). BK2R activation reduced fibrosis in animal models of tubule-interstitial fibrosis (Seccia et al, 2006), and investigators observed increased albuminuria and glomerular sclerosis in a BK2R-deficient Akita mouse model of diabetes (Kakoki et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Bradykinin Decreases Podocyte Permeability through ADAM17-Dependent Epidermal Growth Factor Receptor Activation and Zonula Occludens-1 Rearrangement

Dey

Baldys²,

Sumter³

et al. 2010

J Pharmacol Exp Ther

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Recent data show that increases in bradykinin (BK) concentration contribute to the beneficial effects of angiotensin-converting enzyme inhibitor (ACEI) treatment in chronic kidney disease. However, the possible role of BK in attenuated proteinuria, often seen in ACEI-treated patients, is not well studied. Here, we report that BK decreases mouse podocyte permeability through rearrangement of the tight junction protein zonula occludens-1 (ZO-1) and identify some of the major signaling events leading to permeability change. We show that BK2 receptor (BK2R) stimulation transactivates the epidermal growth factor receptor (EGFR). EGFR transactivation is mediated by a disintegrin and metalloenzyme (ADAM) family members, which are required for both extracellular signalregulated kinase (ERK) and EGFR activation by BK. Using a genesilencing approach we observed that both BK-induced ERK activation and BK-induced permeability decrease in podocytes is attenuated by ADAM17 down-regulation, and we identified epiregulin (ER) as the EGFR ligand participating in ADAM-dependent BK2R-EGFR cross-talk. EGFR inhibition attenuated both ZO-1 rearrangement and BK-induced permeability decreases in podocyte. We propose that ZO-1 redistribution is an important element of BK-induced permeability change and the signaling events involved in ZO-1 rearrangement include transactivation of the EGFR via ADAM17 activation and ER shedding. Our data indicate that ADAM17 and the EGFR may be potential novel therapeutic targets in diabetic nephropathy and other chronic kidney diseases.

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“…Some results suggest that the stimulation of AT2 receptors can evoke a release of kinins from endothelial cells [35,36]. Several effects of ATI receptor antagonists are reduced or abolished by BK B 2 -antagonists suggesting the involvement of kinins [43,44]. Moreover, angiotensin-II-(1-7), the amino-terminal angiotensin heptapeptide, formed from angiotensin I by a recently discovered angiotensin-converting enzyme 2, has a kinin-like activity on the vascular system [35,36,45].…”

Section: Inhibition Of Ace Increase In Insulin Sensitivity and Kininsmentioning

confidence: 99%

The kallikrein‐kinin system, angiotensin converting enzyme inhibitors and insulin sensitivity

Damas

Garbacki

Lefèbvre

2004

Diabetes Metabolism Res

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The therapeutic use of angiotensin converting enzyme (ACE) inhibitors, at a large scale, in arterial hypertension has showed that these molecules can exert beneficial effects on insulin sensitivity and may reduce the occurrence of type 2 diabetes mellitus. One hypothesis explaining these effects of ACE inhibitors may relate to their capacity to interfere with bradykinin (BK) metabolism and action. BK may participate in the regulation of substrate utilization by several tissues by improving blood flow and substrate delivery to the tissues and also by promoting translocation of glucose transporters. Moreover, BK has been shown to increase phosphorylation of insulin receptor and its cell substrates. BK also appears to improve the release of insulin. Furthermore, insulin may activate the kallikrein-kinin system, which consequently may increase its metabolic effects. However, in experimental diabetes mellitus, BK can participate to the inflammatory reaction leading to Langerhans islets destruction. In diabetes, whereas tissue kallikrein mRNA levels were reduced in several organs, an overexpression of kinin receptors, an increase in plasma levels of kininogens and kallikrein and an activation of the kinin system have all been reported. Lastly, kinins may be involved in the development of diabetic nephropathy. Reduction of kinin metabolism by ACE inhibitors might be involved in the beneficial effects exerted by these compounds in diabetic kidney functions.

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Role of Bradykinin in Renoprotective Effects by Angiotensin II Type 1 Receptor Antagonist in Salt-Sensitive Hypertension.

Cited by 8 publications

References 43 publications

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

Effects of Bradykinin on Cardiovascular Remodeling in Renovascular Hypertensive Rats

Bradykinin Decreases Podocyte Permeability through ADAM17-Dependent Epidermal Growth Factor Receptor Activation and Zonula Occludens-1 Rearrangement

The kallikrein‐kinin system, angiotensin converting enzyme inhibitors and insulin sensitivity

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