Effects of Angiotensin II AT1^|^ndash;Receptor Blockade on High Fat Diet^|^ndash;Induced Vascular Oxidative Stress and Endothelial Dysfunction in Dahl Salt-Sensitive Rats

Kosaka, Shinji; Pelisch, Nicolas; Rahman, Matlubur; Nakano, Daisuke; Hitomi, Hirofumi; Kobori, Hiroyuki; Fukuoka, Noriyasu; Kobara, Hideki; Mori, Hideki; Masaki, Tsutomu; Červenka, Luděk; Matsumura, Yasuo; Nishiyama, Akira

doi:10.1254/jphs.12169fp

Cited by 15 publications

(13 citation statements)

References 37 publications

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“…Our result also demonstrated increased plasma Ang II level in HFD-fed mice. It has been reported that Ang II involves in HFD-induced hypertension through various pathways including leptin-related nephropathy [26], restoration of sympathetic over-reactivity [27], megalin-dependent uptake of angiotensinogen into adipocytes [28], vascular oxidative stress and endothelial dysfunction [29], and increased VSM reactivity [131430]. Increased VSM reactivity to Ang II in HFD-fed individuals is reported to be attributed to increased expression of AT1R and ACE 2 [13], and reactive oxygen species (ROS) overproduction and enhanced release of Ca 2+ induced by Ang II [14].…”

Section: Discussionmentioning

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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Section: Discussionmentioning

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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“…In addition, the prevention of target organ damage should be a goal with antihypertensive therapy. The renin-angiotensin system (RAS) regulates blood pressure (3 – 5), reduces sodium excretion (6, 7), and causes kidney damage (8 – 10), and RAS inhibitors are important drugs for treating hypertension or organ damage.…”

Section: Introductionmentioning

confidence: 99%

Angiotensin-Converting Enzyme Inhibitor Does Not Suppress Renal Angiotensin II Levels in Angiotensin I^|^ndash;Infused Rats

et al. 2013

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Angiotensin II (Ang II) infusion into rats elevates local angiotensin II levels through an AT1 receptor–dependent pathway in the kidney. We examined whether treatment with an angio-tensin-converting enzyme (ACE) inhibitor, temocapril, or an AT1-receptor blocker, olmesartan, prevented elevation of Ang II levels in the kidney of angiotensin I (Ang I)-infused rats. Rats were infused with Ang I (100 ng/min) and treated with temocapril (30 mg/kg per day, n = 10) or olmesartan (10 mg/kg per day, n = 9) for 4 weeks. Ang I infusion significantly elevated blood pressure compared with vehicle-infused rats (n = 6). Treatment with temocapril or olmesartan suppressed Ang I–induced hypertension. Temocapril suppressed both plasma and renal ACE activity. Ang I infusion increased Ang II content in the kidney. Interestingly, temocapril failed to reduce the level of Ang II in the kidney, while olmesartan markedly suppressed an increase in renal Ang II levels. These results suggest a limitation of temocapril and a benefit of olmesartan to inhibit the renal renin–angiotensin system and suggest the possible existence of an ACE inhibitor–insensitive pathway that increases Ang II levels in rat kidney.

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“…However, neovascularization need not always be associated with pathological processes. An example of positive impact may be effects on the cardiovascular system in the case of ischemic heart disease (1)(2)(3)(4)(5).…”

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confidence: 99%

The effect of diclofenac on proliferation and production of growth factors by endothelial cells (HMEC-1) under hypoxia and inflammatory conditions

Wiktorowska-Owczarek¹

2014

Acta Pharmaceutica

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Endothelium, which is a dynamic organ, forms a structural barrier between the vascular space and the tissues. Endothelial cells have contact with numerous smooth muscle cells. Many factors such as LDL (low-density lipoproteins), free radicals, infectious microorganisms, shear stress, hypertension, toxins after smoking and/or others may lead to endothelial dysfunction, which is characterized by decreased nitric oxide synthesis. Disturbance in endothelial function is implicated in several diseases, including atherosclerosis, hypertension, inflammatory diseases and cancer metastasis (1-4). Destruction of endothelium by the above-mentioned agents can lead to the release of cytokines and growth factors such as basic fibroblast growth factor (bFGF), which has mitogenic effects on smooth muscle cells (5). The inflammatory process is also responsible for endothelial dysfunction and generation of some growth factors and plays an important role in the progression of atherosclerotic plaque formation. Hypoxia stimulates vascular endothelial growth factor (VEGF) secretion, which is responsible for the formation of new blood

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Effects of Angiotensin II AT1^|^ndash;Receptor Blockade on High Fat Diet^|^ndash;Induced Vascular Oxidative Stress and Endothelial Dysfunction in Dahl Salt-Sensitive Rats

Cited by 15 publications

References 37 publications

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

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

Angiotensin-Converting Enzyme Inhibitor Does Not Suppress Renal Angiotensin II Levels in Angiotensin I^|^ndash;Infused Rats

The effect of diclofenac on proliferation and production of growth factors by endothelial cells (HMEC-1) under hypoxia and inflammatory conditions

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