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home:diseases:hypertension [01.04.2019] – [Recent research] sallieqhome:diseases:hypertension [09.14.2022] (current) – external edit 127.0.0.1
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 +<relatedarticle> [[home:protocol:olmesartan#other beneficial effects|Science behind Olmesartan, section on cardiovascular_disease]] </article>
 ===== Introduction ===== ===== Introduction =====
  
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 Follow your doctor's advice regarding monitoring your blood pressure to determine if your current blood pressure medication/s are effective. Your blood pressure will come down as your Th1 inflammation resolves and you will need less blood pressure medication and then may no longer need additional B/P medication. Your doctor will advise you on how and when to adjust your blood pressure medication/s. Follow your doctor's advice regarding monitoring your blood pressure to determine if your current blood pressure medication/s are effective. Your blood pressure will come down as your Th1 inflammation resolves and you will need less blood pressure medication and then may no longer need additional B/P medication. Your doctor will advise you on how and when to adjust your blood pressure medication/s.
  
-If your B/P is too high, we suggest adding a beta blocker, an ACE inhibitor or a calcium channel blocker (in that order of perference) to your ARB (Benicar).+If your B/P is too high, it is possible to add a beta blocker, an ACE inhibitor or a calcium channel blocker (in that order of perference) to your ARB (Benicar).
  
 ==== If your BP rises on the MP ==== ==== If your BP rises on the MP ====
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 ===== Inflammation and Hypertension ===== ===== Inflammation and Hypertension =====
  
-Hypertension, inflammation and atherosclerosis   (({{pubmed>long:15262906}}))+Hypertension, inflammation and atherosclerosis   (({{pmid>long:15262906}}))
  
  
-Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pubmed>long:16464884}}))+Inflammation may be a bridge connecting hypertension and atherosclerosis. (({{pmid>long:16464884}}))
  
  
-[[http://ndt.oxfordjournals.org/cgi/content/full/21/4/850|Inflammation and hypertension: the search for a link]]+[[https://ndt.oxfordjournals.org/cgi/content/full/21/4/850|Inflammation and hypertension: the search for a link]]
  
 //Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension?// //Elevated high-sensitive C-reactive protein, large arterial stiffness and atherosclerosis: a relationship between inflammation and hypertension?//
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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, and there is now evidence that these actions may be protective for blood vessels.  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, and there is now evidence that these actions may be protective for blood vessels. 
  
-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.     (({{pubmed>long:16481882}}))</blockquote>+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.     (({{pmid>long:16481882}}))</blockquote>
  
 //see also// //see also//
 Nephrol Dial Transplant. 2006 Apr;21(4):850-3. Epub 2006 Feb 7. Nephrol Dial Transplant. 2006 Apr;21(4):850-3. Epub 2006 Feb 7.
 Inflammation and hypertension: the search for a link. Inflammation and hypertension: the search for a link.
-Pauletto P, Rattazzi M.    (({{pubmed>long:16464884}}))+Pauletto P, Rattazzi M.    (({{pmid>long:16464884}}))
  
  
  
-Wilke, R. A., R. U. Simpson, et al. (2009). "Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension." Pharmacogenomics 10(11): 1789-1797.   (({{pubmed>long:19891555}}))+Wilke, R. A., R. U. Simpson, et al. (2009). "Genetic variation in CYP27B1 is associated with congestive heart failure in patients with hypertension." Pharmacogenomics 10(11): 1789-1797.   (({{pmid>long:19891555}}))
 <blockquote> <blockquote>
  
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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'Agostino characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.” (({{pubmed>long:11714414}}))</blockquote>+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'Agostino characterizes hypertension in this way: “There is no reason to believe that hypertension is simply elevated blood pressure. Hypertension is much more complex.” (({{pmid>long:11714414}}))</blockquote>
  
 __ __
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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>long:25001274}}))+pressure, compared with 20 mg.      (({{pmid>long:25001274}}))
  
  
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 ===== Recent research ===== ===== Recent research =====
  
-Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients.  (({{pubmed>long:29462508}}))+Comparative effectiveness of an angiotensin receptor blocker, olmesartan medoxomil, in older hypertensive patients.  (({{pmid>long:29462508}}))
  
  
-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>long:21061834}}))+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>long:21061834}}))
  
  
-Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.   (({{pubmed>long:21063874}}))+Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.   (({{pmid>long:21063874}}))
  
-Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground.  (({{pubmed>long:21504378}}))+Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the olmesartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground.  (({{pmid>long:21504378}}))
  
 {{tag>disease symptoms }} {{tag>disease symptoms }}
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 +<nodisp>
 ===== Notes and comments ===== ===== Notes and comments =====
  
-//BROKEN LINK// [[http://hyper.ahajournals.org/cgi/content/full/44/3/253|Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?]]+//BROKEN LINK// [[https://hyper.ahajournals.org/cgi/content/full/44/3/253|Is Vascular Endothelial Growth Factor a Missing Link Between Hypertension and Inflammation?]]
  
 ANOR //DEAD LINK//  ANOR //DEAD LINK// 
-[[http://hyper.ahajournals.org/content/hypertensionaha/early/2014/07/07/HYPERTENSIONAHA.114.03282.full.pdf|Dose-Dependent  Arterial  Destiffening  and  Inward  +[[https://hyper.ahajournals.org/content/hypertensionaha/early/2014/07/07/HYPERTENSIONAHA.114.03282.full.pdf|Dose-Dependent  Arterial  Destiffening  and  Inward  
 Remodeling  After  Olmesartan  in  Hypertensives  With   Remodeling  After  Olmesartan  in  Hypertensives  With  
 Metabolic  Syndrome]] Metabolic  Syndrome]]
  
-link to current research by 2 authers [[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Savoia%20C%22[Author]|Savoia C]], [[http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Schiffrin%20EL%22[Author]|Schiffrin EL.]]+link to current research by 2 authers [[https://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Savoia%20C%22[Author]|Savoia C]], [[https://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed&cmd=Search&itool=pubmed_Abstract&term=%22Schiffrin%20EL%22[Author]|Schiffrin EL.]]
  
 Vitamins  Vitamins 
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 --- //Sallie Q 02.22.2017//  moved contents of 1st para out of view as follows --- //Sallie Q 02.22.2017//  moved contents of 1st para out of view as follows
  
-http://www.newswire.ca/en/releases/archive/May2009/21/c6035.html+https://www.newswire.ca/en/releases/archive/May2009/21/c6035.html
  
  
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   *Legacy content   *Legacy content
  
-http://www.lipidsonline.org/news/article.cfm?aid=9682+https://www.lipidsonline.org/news/article.cfm?aid=9682
  
  
  
-  * **salt avoidance** – not recommended given that the body seems to naturally regulate sodium levels independently(({{pubmed>long:19833911}}))+  * **salt avoidance** – not recommended given that the body seems to naturally regulate sodium levels independently(({{pmid>long:19833911}}))
  
  
-<blockquote>Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women. (({{pubmed>long:21061834}}))+<blockquote>Effects of olmesartan vs irbesartan on metabolic parameters and visfatin in hypertensive obese women. (({{pmid>long:21061834}}))
  
-http://www.ncbi.nlm.nih.gov/pubmed/21061834 (USED on page --- //Sallie Q 01.04.2019// )+https://www.ncbi.nlm.nih.gov/pubmed/21061834 (USED on page --- //Sallie Q 01.04.2019// )
  
 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://www.dmsjournal.com/content/2/1/21+https://www.dmsjournal.com/content/2/1/21
  
 Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, and possibly in insulin secretion. Its physiology has begun to be described but its role on diabetes and CAD pathophysiology is still controversial. Visfatin is is an adipokine involved in inflammatory phenomena, atherosclerosis, and possibly in insulin secretion. Its physiology has begun to be described but its role on diabetes and CAD pathophysiology is still controversial.
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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>long:21063874}}))+Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients. (({{pmid>long:21063874}}))
  
-http://www.ncbi.nlm.nih.gov/pubmed/21063874+https://www.ncbi.nlm.nih.gov/pubmed/21063874
  
 Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP. Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP.
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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: 142-156/94-98 mmHg) were treated with olmesartan medoxomil (20 mg/day for 6 months) and blood samples collected at baseline, 3 and 6 months for PBMC p22(phox) and HO-1 protein expression, phosphorylation state of ERK1/2 (western blot) and oxLDL level (ELISA) evaluations. Olmesartan normalized blood pressure since the third month (149 ± 4.7/94.88 ± 1.9 mmHg vs 137.89 ± 2.08/88.44 ± 2.0 at 3 months and vs 135.44 ± 2.18/85.78 ± 1.2 at 6 months, analysis of variance: p < 0.001). p22(phox) protein level declined at 3 months (7.10 ± 2.61 vs 9.32 ± 2.43 densitometric units (d.u.; p < 0.001), further declining at 6 months (4.55 ± 1.26 d.u., p < 0.001). HO-1 levels increased at 3 months (10.87 ± 1.92 vs 7.70 ± 0.71 d.u., p = 0.001) and remained elevated (11.11 ± 1.89 d.u., p = 0.001), without further increase at 6 months. Phosphorylated ERK1/2 declined at 3 months (3.94 ± 1.44 vs 5.62 ± 1.11 d.u., p = 0.001), further declining at 6 months (1.94 ± 0.87, p < 0.001). oxLDL significantly declined at 3 and 6 months. These results demonstrate that olmesartan inhibits oxidative stress. Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground.  (({{pubmed>long:21504378}}))+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: 142-156/94-98 mmHg) were treated with olmesartan medoxomil (20 mg/day for 6 months) and blood samples collected at baseline, 3 and 6 months for PBMC p22(phox) and HO-1 protein expression, phosphorylation state of ERK1/2 (western blot) and oxLDL level (ELISA) evaluations. Olmesartan normalized blood pressure since the third month (149 ± 4.7/94.88 ± 1.9 mmHg vs 137.89 ± 2.08/88.44 ± 2.0 at 3 months and vs 135.44 ± 2.18/85.78 ± 1.2 at 6 months, analysis of variance: p < 0.001). p22(phox) protein level declined at 3 months (7.10 ± 2.61 vs 9.32 ± 2.43 densitometric units (d.u.; p < 0.001), further declining at 6 months (4.55 ± 1.26 d.u., p < 0.001). HO-1 levels increased at 3 months (10.87 ± 1.92 vs 7.70 ± 0.71 d.u., p = 0.001) and remained elevated (11.11 ± 1.89 d.u., p = 0.001), without further increase at 6 months. Phosphorylated ERK1/2 declined at 3 months (3.94 ± 1.44 vs 5.62 ± 1.11 d.u., p = 0.001), further declining at 6 months (1.94 ± 0.87, p < 0.001). oxLDL significantly declined at 3 and 6 months. These results demonstrate that olmesartan inhibits oxidative stress. Given the involvement of oxidative stress and its signaling in atherogenesis, and the available evidence of olmesartan's vasoprotective, anti-inflammatory and antiatherosclerotic effects derived from clinical trials in humans, the results of our study provide a mechanistic rationale for the omelsartan's antioxidant and anti-inflammatory potential translation, in the long term, toward the antiatherosclerotic and antiremodeling effects reported on the clinical ground.  (({{pmid>long:21504378}}))
  
 PMID: PMID:
-21504378 (part  USED on page --- //Sallie Q 01.04.2019//</blockquote> +21504378 (part  USED on page --- //Sallie Q 01.04.2019//</blockquote> </nodisp> 
home/diseases/hypertension.txt · Last modified: 09.14.2022 by 127.0.0.1
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