Heat shock augments angiotensin II-induced vascular contraction through increased production of reactive oxygen species

Kim, Jee In; Jung, Sang Won; Yang, Enyue; Park, Kwon Moo; Eto, Masumi; Kim, In Kyeom

doi:10.1016/j.bbrc.2010.07.115

Cited by 9 publications

(6 citation statements)

References 36 publications

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“…It is well-known that in the blood vessel wall AngII is a potent stimulator of ROS including O À 2 (Berry et al 2000) and H 2 O 2 (Zafari et al 1998). Both of these ROS are known to mediate AngII-induced vasoconstriction (Kawazoe et al 1999, Torrecillas et al 2001, Shastri et al 2002, de Groot et al 2004, Puntmann et al 2005, Hussain et al 2006, Bagi et al 2008, Kim et al 2010, Pfister et al 2011. Quenching of O À 2 with PEG-SOD blunted AngII reactivity similarly in SS-13 BN rats on normal diet and hypercaloric diet, whereas H 2 O 2 -mediated AngII reactivity was only present in aortas from SS-13 BN rats on hypercaloric diet.…”

Section: Discussionmentioning

confidence: 98%

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

2012

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Aim To test the hypothesis that hyper-caloric diet on mechanisms of angiotensin (Ang)II-induced vasoconstriction in Dahl salt-sensitive (SS) rats and genetic control SS-13BN rats. Methods Aortic function was assessed using wire myography in 16-week-old rats maintained on a normal diet or started on a 4-week hyper-caloric diet at 12-weeks-old. Results On normal diet, AngII vasoconstriction was greater in SS rats than SS-13BN rats. Intriguingly, the AngII response was reduced in aortic rings from SS rats on hyper-caloric diet versus normal diet, whereas this response was not altered by hyper-caloric diet in SS-13BN rats. We probed whether O2−, H2O2, or NO mediate the AngII response. PEG-SOD reduced the AngII response in all 4 groups. Catalase treatment of aortic rings did not alter aortic AngII response from SS rats on hyper-caloric but reduced the aortic AngII response of SS rats on normal diet; the exact opposite finding was observed with catalase in SS-13BN rats. L-NAME increased AngII response in SS rats on hyper-caloric but was without effect in the normal diet group. In stark contrast, L-NAME did not alter the AngII response in SS-13BN rats on hyper-caloric diet, yet L-NAME enhanced AngII responsiveness in the normal diet group. In SS rats, hyper-caloric diet increased aortic NOS3 activity and expression corresponding with increased endothelial-dependent vasorelaxation. Conclusion A short-term hyper-caloric diet elicits a vasodilatory phenotype in SS rats, but not in SS-13BN rats, by increasing NOS3 expression and function as well as reducing H2O2 function.

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Section: Discussionmentioning

confidence: 98%

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

2012

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“…It was reported that AT 2 receptor stimulation interacted with AT 1 receptor stimulation (34), which activated NADPH oxidase (10,24). Furthermore, it was recently demonstrated that a heat shock-induced ROS production augmented ANG II-induced contraction in aorta (18). Therefore it might be possible that TSA inhibits the increased ANG II-induced contraction presumably via inhibition of ROS production through AT 2 receptor blockade.…”

Section: Discussionmentioning

confidence: 99%

HDAC4 mediates development of hypertension via vascular inflammation in spontaneous hypertensive rats

Usui

Okada

Mizuno

et al. 2012

American Journal of Physiology-Heart and Circulatory Physiology

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Our recent study demonstrated that HDAC4 protein specifically increases in mesenteric artery from spontaneous hypertensive rats (SHR) compared with Wistar Kyoto rats (WKY). Vascular inflammation is important for pathogenesis of hypertension. We examined whether HDAC4 affects vascular inflammatory responses and promotes hypertension. In vivo, blood pressure, reactive oxygen species (ROS) production, and VCAM-1 expression in isolated mesenteric artery were elevated in young SHR (7 wk old) compared with age-matched WKY, which were prevented by long-term treatment of SHR with an HDACs inhibitor, trichostatin A (TSA; 500 g·kg Ϫ1 ·day Ϫ1 for 3 wk). In isolated mesenteric artery, the increased angiotensin II-induced contraction in SHR was reversed by TSA. The endothelium-dependent relaxation induced by ACh in SHR was augmented by TSA. In cultured rat mesenteric arterial smooth muscle cells (SMCs), expression of HDAC4 mRNA and protein was increased by TNF-␣ (10 ng/ml). TSA (10 M, pretreatment for 30 min) inhibited VCAM-1 expression and NF-B phosphorylation induced by TNF (10 ng/ml, 24 h or 20 min) in SMCs. HDAC4 small interfering RNA inhibited TNF-induced monocyte adhesion, VCAM-1 expression, transcriptional activity of NF-B, and ROS production in SMCs. The present results demonstrated that proinflammatory effects of HDACs may mediate the further development of hypertension in SHR. It is also suggested in cultured vascular SMCs that TNF-induced HDAC4 mediates vascular inflammation likely via VCAM-1 induction through ROS-dependent NF-B activation. oxygen radicals; smooth muscle; contractile function CAM IS ASSOCIATED WITH A VARIETY of cell functions including inflammation, apoptosis, and muscular contraction. Recent evidence indicates that CaM-related proteins are responsible for cardiovascular diseases. In the previous study, we compared expression levels of six CaM-related proteins with almost unknown functions in vasculature [CaMKII␦, eukaryotic elongation factor 2 kinase (eEF2K; also known as CaMKIII), histone deacetylase (HDAC)4, HDAC5, death associated protein kinase (DAPK)3, and CaM serine kinase (CASK)] in aorta and mesenteric artery from spontaneous hypertensive rats (SHR) and Wistar Kyoto rats (WKY) (48). As a result, we for the first time demonstrated that expressions of eEF2K, HDAC4, and DAPK3 protein increased in SHR compared with WKY. However, it remained to be clarified how each CaM-related protein might affect vascular pathophysiology and control the development of hypertension.HDACs have been considered as transcriptional corepressors that catalyze histone deacetylation in diverse physiological systems (33, 42). Up to now, HDACs have been classified into four groups termed class I HDACs (HDAC1, 2, 3, and 8), class II HDACs (HDAC4, 5, 6, 7, 9, and 10), class III HDACs, and class IV HDAC (HDAC11). The class II HDACs are further divided into the class IIa (HDAC4, 5, 7, 9) and the class IIb (HDAC6 and 10) (26). A recent study clarified that the class I and IIa HDACs play critical roles in mediating cardiac h...

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“…Protein samples were prepared and western blot analysis were performed as previously described [18]. Protein samples were electrophoresed on 10~12% polyacrylamide gel with 0.1% SDS and transferred to PVDF membranes, and then subjected to an immunoblotting with antibodies against pMLC at Thr18 and Ser19 (Santa Cruz, CA, USA ), p-MYPT1 at Thr853 (Santa Cruz, CA, USA), p-CPI-17 at Thr38 (Millipore, Darmstadt, Germany), and MLCK (Santa Cruz, CA, USA).…”

Section: Methodsmentioning

confidence: 99%

High fat diet confers vascular hyper-contractility against angiotensin II through upregulation of MLCK and CPI-17

Kim

2017

Korean J Physiol Pharmacol

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Obesity is a critical risk factor for the hypertension. Although angiotensin II (Ang II) in obese individuals is known to be upregulated in obesity-induced hypertension, direct evidence that explains the underlying mechanism for increased vascular tone and consequent increase in blood pressure (BP) is largely unknown. The purpose of this study is to investigate the novel mechanism underlying Ang II-induced hyper-contractility and hypertension in obese rats. Eight-week old male Sprague-Dawley rats were fed with 60% fat diet or normal diet for 4 months. Body weight, plasma lipid profile, plasma Ang II level, BP, Ang II-induced vascular contraction, and expression of regulatory proteins modulating vascular contraction with/without Ang II stimulation were measured. As a result, high fat diet (HFD) accelerated age-dependent body weight gaining along with increased plasma Ang II concentration. It also increased BP and Ang II-induced aortic contraction. Basal expression of p-CPI-17 and myosin light chain (MLC) kinase was increased by HFD along with increased phosphorylation of MLC. Ang II-induced phosphorylation of CPI-17 and MLC were also higher in HFD group than control group. In conclusion HFD-induced hypertension is through at least in part by increased vascular contractility via increased expression and activation of contractile proteins and subsequent MLC phosphorylation induced by increased Ang II.

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Heat shock augments angiotensin II-induced vascular contraction through increased production of reactive oxygen species

Cited by 9 publications

References 36 publications

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

HDAC4 mediates development of hypertension via vascular inflammation in spontaneous hypertensive rats

High fat diet confers vascular hyper-contractility against angiotensin II through upregulation of MLCK and CPI-17

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