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home:diseases:hypertension [03.30.2020] – [Hypertension (high blood pressure)] sallieq | home:diseases:hypertension [09.14.2022] (current) – external edit 127.0.0.1 | ||
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====== Hypertension (high blood pressure) ====== | ====== Hypertension (high blood pressure) ====== | ||
- | https:// | ||
- | < | + | |
+ | < | ||
===== Introduction ===== | ===== Introduction ===== | ||
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===== Inflammation and Hypertension ===== | ===== Inflammation and Hypertension ===== | ||
- | Hypertension, | + | Hypertension, |
- | Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pubmed> | + | Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pmid> |
- | [[http:// | + | [[https:// |
//Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: | //Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: | ||
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RECENT FINDINGS: Essential hypertension is characterized by increased peripheral vascular resistance to blood flow, due in large part to vascular remodeling. Vascular changes in hypertension are associated with mechanical and humoral factors that modulate signaling events, resulting in abnormal function, media growth, extracellular matrix deposition and inflammation. Recent evidence suggests that inflammation is present in the vasculature in animal models of hypertension. Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome. In animal and human studies, pro-inflammatory components of the renin-angiotensin-aldosterone system have been demonstrated in large conduit and small arteries in the kidney and heart. Peroxisome proliferator-activated receptor activators are drugs with metabolic properties that have been demonstrated to exert anti-inflammatory effects on the vasculature, | RECENT FINDINGS: Essential hypertension is characterized by increased peripheral vascular resistance to blood flow, due in large part to vascular remodeling. Vascular changes in hypertension are associated with mechanical and humoral factors that modulate signaling events, resulting in abnormal function, media growth, extracellular matrix deposition and inflammation. Recent evidence suggests that inflammation is present in the vasculature in animal models of hypertension. Inflammatory markers, such as C-reactive protein, are associated with vascular lesions in humans, and are predictive of cardiovascular outcome. In animal and human studies, pro-inflammatory components of the renin-angiotensin-aldosterone system have been demonstrated in large conduit and small arteries in the kidney and heart. Peroxisome proliferator-activated receptor activators are drugs with metabolic properties that have been demonstrated to exert anti-inflammatory effects on the vasculature, | ||
- | SUMMARY: Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension and its complications. | + | SUMMARY: Inflammatory processes are important participants in the pathophysiology of hypertension and cardiovascular disease. The identification of the mechanisms leading to the activation of inflammation should contribute to the development of specific therapeutic approaches to apply in hypertension and its complications. |
//see also// | //see also// | ||
Nephrol Dial Transplant. 2006 Apr; | Nephrol Dial Transplant. 2006 Apr; | ||
Inflammation and hypertension: | Inflammation and hypertension: | ||
- | Pauletto P, Rattazzi M. (({{pubmed> | + | Pauletto P, Rattazzi M. (({{pmid> |
- | Wilke, R. A., R. U. Simpson, et al. (2009). " | + | Wilke, R. A., R. U. Simpson, et al. (2009). " |
< | < | ||
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- | For some, the absence of well-defined causal connections between diseases and surrogate outcomes is a tribute to how truly complicated chronic inflammatory diseases are. Ralph B D' | + | For some, the absence of well-defined causal connections between diseases and surrogate outcomes is a tribute to how truly complicated chronic inflammatory diseases are. Ralph B D' |
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intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able | intrinsic elastic properties of the carotid artery wall material. These data suggest that 40 and 80 mg olmesartan were able | ||
to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood | to significantly remodel and destiffen the arterial wall material during long-term treatment, partly independently of blood | ||
- | pressure, compared with 20 mg. (({{pubmed> | + | pressure, compared with 20 mg. (({{pmid> |
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===== Recent research ===== | ===== Recent research ===== | ||
- | Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients. | + | Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients. |
- | The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. (({{pubmed> | + | The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. (({{pmid> |
- | Olmesartan ameliorated arterial stiffness in patients with hypertension, | + | Olmesartan ameliorated arterial stiffness in patients with hypertension, |
- | Given the involvement of oxidative stress and its signaling in atherogenesis, | + | Given the involvement of oxidative stress and its signaling in atherogenesis, |
{{tag> | {{tag> | ||
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+ | < | ||
===== Notes and comments ===== | ===== Notes and comments ===== | ||
- | //BROKEN LINK// [[http:// | + | //BROKEN LINK// [[https:// |
ANOR //DEAD LINK// | ANOR //DEAD LINK// | ||
- | [[http:// | + | [[https:// |
Remodeling | Remodeling | ||
Metabolic | Metabolic | ||
- | link to current research by 2 authers [[http:// | + | link to current research by 2 authers [[https:// |
Vitamins | Vitamins | ||
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--- //Sallie Q 02.22.2017// | --- //Sallie Q 02.22.2017// | ||
- | http:// | + | https:// |
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*Legacy content | *Legacy content | ||
- | http:// | + | https:// |
- | * **salt avoidance** – not recommended given that the body seems to naturally regulate sodium levels independently(({{pubmed> | + | * **salt avoidance** – not recommended given that the body seems to naturally regulate sodium levels independently(({{pmid> |
- | < | + | < |
- | http:// | + | https:// |
CONCLUSION: The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. | CONCLUSION: The administration of olmesartan improved blood pressure, insulin, HOMA, visfatin and lipid profile in hypertensive obese women. Irbesartan improved blood pressure and lipid levels. | ||
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Visfatin, glucose metabolism and vascular disease: a review of evidence | Visfatin, glucose metabolism and vascular disease: a review of evidence | ||
- | http:// | + | https:// |
Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, | Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, | ||
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~~~~ | ~~~~ | ||
(part below ref. USED on page --- --- //Sallie Q 01.04.2019// | (part below ref. USED on page --- --- //Sallie Q 01.04.2019// | ||
- | Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. (({{pubmed> | + | Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. (({{pmid> |
- | http:// | + | https:// |
Olmesartan ameliorated arterial stiffness in patients with hypertension, | Olmesartan ameliorated arterial stiffness in patients with hypertension, | ||
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Abstract | Abstract | ||
- | Abstract The role of oxidative stress in the pathophysiology of hypertension and target organ damage is widely recognized. Using a molecular biology approach, we report, in essential hypertensive patients, the effect of the angiotensin II type 1 receptor blocker olmesartan on the mononuclear cell (PBMC) protein expression of major elements in the oxidative stress and vascular remodeling-related pathways, p22(phox) and HO-1, along with the phosphorylation state of ERK1/2 and plasma oxidized low-density lipoproteins (oxLDL). Twenty untreated essential hypertensive patients (range blood pressure: 142-156/ | + | Abstract The role of oxidative stress in the pathophysiology of hypertension and target organ damage is widely recognized. Using a molecular biology approach, we report, in essential hypertensive patients, the effect of the angiotensin II type 1 receptor blocker olmesartan on the mononuclear cell (PBMC) protein expression of major elements in the oxidative stress and vascular remodeling-related pathways, p22(phox) and HO-1, along with the phosphorylation state of ERK1/2 and plasma oxidized low-density lipoproteins (oxLDL). Twenty untreated essential hypertensive patients (range blood pressure: 142-156/ |
PMID: | PMID: | ||
- | 21504378 (part USED on page --- //Sallie Q 01.04.2019//</ | + | 21504378 (part USED on page --- //Sallie Q 01.04.2019//</ |