Difference between revisions of "Hypertension"

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<h3>Alpha-adrenergic system</h3>
 
<h3>Alpha-adrenergic system</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15288883">PMID: 15288883</a><br /></div>
 
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<h3>Vessel wall stiffness</h3>
 
<h3>Vessel wall stiffness</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/22290157">PMID: 22290157</a><br /></div>
 
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<h3>Na, K - ATPase</h3>
 
<h3>Na, K - ATPase</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/1647122">PMID: 1647122</a><br /></div>
 
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<h3>Smooth muscle cells  Of vessel wall</h3>
 
<h3>Smooth muscle cells  Of vessel wall</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15194174">PMID: 15194174</a><br /></div>
 
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<h3>Left ventricular hypertrophy</h3>
 
<h3>Left ventricular hypertrophy</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/1533758">PMID: 1533758</a><br /></div>
 
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</div>(...)<!--Pop-up for: Renin-angiotensin system !Pop-up-->
 
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<h3>Renin-angiotensin system</h3>
 
<h3>Renin-angiotensin system</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/24592256">PMID: 24592256</a><br /></div>
 
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<h3>Activation of sympathetic nervous system</h3>
 
<h3>Activation of sympathetic nervous system</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19874988">PMID: 19874988</a><br /></div>
 
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</div>(...)<!--Pop-up for: Baroreceptors  Sensitivity failure !Pop-up-->
 
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<h3>Baroreceptors  Sensitivity failure</h3>
 
<h3>Baroreceptors  Sensitivity failure</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/5080421">PMID: 5080421</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/24058186">PMID: 24058186</a><br /></div>
 
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<h3>Diastolic dysfunction</h3>
 
<h3>Diastolic dysfunction</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/12151871">PMID: 12151871</a><br /></div>
 
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</div>(...)<!--Pop-up for: Insulin-dependent Vasodilation failure !Pop-up-->
 
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<h3>Insulin-dependent Vasodilation failure</h3>
 
<h3>Insulin-dependent Vasodilation failure</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/9590566">PMID: 9590566</a><br /></div>
 
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<h3>Reduced level of NO</h3>
 
<h3>Reduced level of NO</h3>
<div class="links"> </div>
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<div class="links"><a href=" ">Reduced level of NO</a><br /></div>
 
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</div>(...)<!--Pop-up for: Insulin resistance !Pop-up-->
 
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<h3>Insulin resistance</h3>
 
<h3>Insulin resistance</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/2405235">PMID: 2405235</a><br /></div>
 
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</div>(...)<!--Pop-up for: Terminal renal failure !Pop-up-->
 
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<h3>Terminal renal failure</h3>
 
<h3>Terminal renal failure</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15252775">PMID: 15252775</a><br /></div>
 
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<h3>Diabetes mellitus</h3>
 
<h3>Diabetes mellitus</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11304502">PMID: 11304502</a><br /></div>
 
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<h3>Excess consumption  Of NaCl</h3>
 
<h3>Excess consumption  Of NaCl</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/25398734">PMID: 25398734</a><br /></div>
 
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</div>(...)<!--Pop-up for: Hypertension  !Pop-up-->
 
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<div class="1HWTN2RG5-24TF7C2-19S" style="display:none;">
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<h3>Hypertension </h3>
 
<h3>Hypertension </h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/10721957">PMID: 10721957</a><br /></div>
 
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<h3>Mini-strokes</h3>
 
<h3>Mini-strokes</h3>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16357086">PMID: 16357086</a><br /></div>
 
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</div>(...)<!--Pop-up for: Hypertrophy of left atrium !Pop-up-->
 
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<h3>Hypertrophy of left atrium</h3>
 
<h3>Hypertrophy of left atrium</h3>
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<div class="links"><a href=" ">Hypertrophy of left atrium</a><br /></div>
 
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<h3>elastin crosslinks</h3>
 
<h3>elastin crosslinks</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/22290157">PMID: 22290157</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/20590836">PMID: 20590836</a><br /></div>
 
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<h3>brain dysfunction</h3>
 
<h3>brain dysfunction</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/16357086">PMID: 16357086</a><br /></div>
 
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</div>(...)<!--Pop-up for: Lipid metabolism failure !Pop-up-->
 
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<h3>Lipid metabolism failure</h3>
 
<h3>Lipid metabolism failure</h3>
<div class="links"> </div>
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<div class="links"><a href=" ">Lipid metabolism failure</a><br /></div>
 
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<h3>Vasoconstriction </h3>
 
<h3>Vasoconstriction </h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/19297247">PMID: 19297247</a><br /></div>
 
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<h3>Extracellular calcium</h3>
 
<h3>Extracellular calcium</h3>
<div class="links"> </div>
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<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/9536295">PMID: 9536295</a><br /></div>
 
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</div>(...)<!--Pop-up for: Cardiac pathology !Pop-up-->
 
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<h3>Cardiac pathology</h3>
 
<h3>Cardiac pathology</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/10721957">PMID: 10721957</a><br /></div>
 
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</div>(...)<!--Pop-up for: Oxidative stress !Pop-up-->
 
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<h3>Oxidative stress</h3>
 
<h3>Oxidative stress</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/15262903">PMID: 15262903</a><br /></div>
 
</div>(...)<!--Pop-up for: NO-dependent vasodilation failure !Pop-up-->
 
</div>(...)<!--Pop-up for: NO-dependent vasodilation failure !Pop-up-->
 
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<h3>NO-dependent vasodilation failure</h3>
 
<h3>NO-dependent vasodilation failure</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/25343007">PMID: 25343007</a><br /></div>
 
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</div>(...)<!--Pop-up for: Inflammation !Pop-up-->
 
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<h3>Inflammation</h3>
 
<h3>Inflammation</h3>
<div class="links"> </div>
+
<div class="links"><a href=" ">Inflammation</a><br /></div>
 
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</div>(...)<!--Pop-up for: Glycation !Pop-up-->
 
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<h3>Glycation</h3>
 
<h3>Glycation</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/20590836">PMID: 20590836</a><br /></div>
 
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</div>(...)<!--Pop-up for: Increased secretion of endothelin !Pop-up-->
 
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<h3>Increased secretion of endothelin</h3>
 
<h3>Increased secretion of endothelin</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/25405182">PMID: 25405182</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/25239727">PMID: 25239727</a><br /></div>
 
</div>(...)<!--Pop-up for: Osteoporosis !Pop-up-->
 
</div>(...)<!--Pop-up for: Osteoporosis !Pop-up-->
 
<div class="1HWTPDTMF-2342153-2JS" style="display:none;">
 
<div class="1HWTPDTMF-2342153-2JS" style="display:none;">
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<h3>Osteoporosis</h3>
 
<h3>Osteoporosis</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/9536295">PMID: 9536295</a><br /><a href="http://www.ncbi.nlm.nih.gov/pubmed/24060147">PMID: 24060147</a><br /></div>
 
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</div>(...)<!--Pop-up for: Nonesterified fatty acids !Pop-up-->
 
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<h3>Nonesterified fatty acids</h3>
 
<h3>Nonesterified fatty acids</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/11276390">PMID: 11276390</a><br /></div>
 
</div>(...)<!--Pop-up for: Renal insufficiency !Pop-up-->
 
</div>(...)<!--Pop-up for: Renal insufficiency !Pop-up-->
 
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<div class="1HWTPWP8N-1F81RKT-37R" style="display:none;">
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<h3>Renal insufficiency</h3>
 
<h3>Renal insufficiency</h3>
<div class="links"> </div>
+
<div class="links"></div>
 
</div>(...)<!--Pop-up for: Peripheral resistance !Pop-up-->
 
</div>(...)<!--Pop-up for: Peripheral resistance !Pop-up-->
 
<div class="1HWTN26HZ-BZC43D-17T" style="display:none;">
 
<div class="1HWTN26HZ-BZC43D-17T" style="display:none;">
 +
  
  
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<h3>Peripheral resistance</h3>
 
<h3>Peripheral resistance</h3>
<div class="links"> </div>
+
<div class="links"><a href="http://www.ncbi.nlm.nih.gov/pubmed/25343007">PMID: 25343007</a><br /></div>
</div>(.//.)(.//.)<!-- Do not edit!  -->
+
</div>(.//.)<h1>Hypertension </h1>
 +
 
 +
<p>High blood pressure, also known as hypertension, is 1 of the most well-known major risk factors for cardiovascular disease (CVD) and stroke. Estimates reported by the American Heart Association indicate that in 2007–2010, 33% of all adults aged ≥20 years in the United States had hypertension. Dietary interventions, in particular those based on sodium or potassium intakes, have demonstrated their ability to reduce blood pressure in humans. Two recently published meta-analyses reported that lower sodium intake resulted in lower levels of blood pressure.</p>
 +
<p>Metabolic disorders, such as obesity and non-insulin-dependent diabetes mellitus, and cardiovascular disorders, such as essential hypertension, congestive cardiac failure and atherosclerosis, have two features in common, namely relative resistance to insulin-mediated glucose uptake and vascular endothelial dysfunction. Significant increases in limb blood flow occur in response to systemic hyperinsulinaemia, although there is marked variation in the results due to a number of confounding factors, including activation of the sympathetic nervous system. Local hyperinsulinaemia has a less marked vasodilator action. Insulin may stimulate endothelial nitric oxide production or may act directly on vascular smooth muscle via stimulation of the Na+-H+ exchanger and Na+/K+-ATPase, leading to hyperpolarization of the cell membrane and consequent closure of voltage-gated Ca2+ channels. Skeletal muscle blood flow is a determinant of glucose uptake so endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of hypertension with insulin resistance. A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake is central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease. </p>
 +
<p>Osteoporosis is closely connected with hypertension. One of the important function of the bone is a metabolic function as a storehouse for calcium. In osteoporosis, this second function of the bone is also lost, because there is less space available for calcium storage. Calcium deficiency becomes more and more pronounced as we age, due to a reduced calcium intake, poorer intestinal absorption, lower 1,25(OH)2 vitamin D levels because of shorter solar exposure and declining renal function. Secondary hyperparathyroidism would be an unavoidable consequence of aging unless sufficient calcium and/or vitamin D were provided. Since excess PTH removes calcium from bone by stimulating bone resorption, bone mass decreases leading to osteoporosis. In addition, calcium entering soft tissues such as blood vessels and brain, especially the intracellular compartment, may cause functional deterioration of these organs causing hypertension, arteriosclerosis and senile dementia. </p>
 +
<p>The kidney and vasculature are rich sources of NADPH oxidase–derived ROS, which under pathological conditions play an important role in renal dysfunction and vascular damage. Strong experimental evidence indicates that increased oxidative stress and associated oxidative damage are mediators of renovascular injury in cardiovascular pathologies. Increased production of superoxide anion and hydrogen peroxide, reduced nitric oxide synthesis, and decreased bioavailability of antioxidants have been demonstrated in experimental and human hypertension.</p>
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Revision as of 14:17, 17 June 2015

This is a graph with borders and nodes. Maybe there is an Imagemap used so the nodes may be linking to some Pages.

Hypertension 

High blood pressure, also known as hypertension, is 1 of the most well-known major risk factors for cardiovascular disease (CVD) and stroke. Estimates reported by the American Heart Association indicate that in 2007–2010, 33% of all adults aged ≥20 years in the United States had hypertension. Dietary interventions, in particular those based on sodium or potassium intakes, have demonstrated their ability to reduce blood pressure in humans. Two recently published meta-analyses reported that lower sodium intake resulted in lower levels of blood pressure.

Metabolic disorders, such as obesity and non-insulin-dependent diabetes mellitus, and cardiovascular disorders, such as essential hypertension, congestive cardiac failure and atherosclerosis, have two features in common, namely relative resistance to insulin-mediated glucose uptake and vascular endothelial dysfunction. Significant increases in limb blood flow occur in response to systemic hyperinsulinaemia, although there is marked variation in the results due to a number of confounding factors, including activation of the sympathetic nervous system. Local hyperinsulinaemia has a less marked vasodilator action. Insulin may stimulate endothelial nitric oxide production or may act directly on vascular smooth muscle via stimulation of the Na+-H+ exchanger and Na+/K+-ATPase, leading to hyperpolarization of the cell membrane and consequent closure of voltage-gated Ca2+ channels. Skeletal muscle blood flow is a determinant of glucose uptake so endothelial dysfunction, resulting in a relative inability of mediators, including insulin, to stimulate muscle blood flow, may be the underlying mechanism accounting for the association of hypertension with insulin resistance. A complex interaction between endothelial dysfunction, abnormal skeletal muscle blood flow and reduced insulin-mediated glucose uptake is central to the link between insulin resistance, blood pressure, impaired glucose tolerance and the risk of cardiovascular disease.

Osteoporosis is closely connected with hypertension. One of the important function of the bone is a metabolic function as a storehouse for calcium. In osteoporosis, this second function of the bone is also lost, because there is less space available for calcium storage. Calcium deficiency becomes more and more pronounced as we age, due to a reduced calcium intake, poorer intestinal absorption, lower 1,25(OH)2 vitamin D levels because of shorter solar exposure and declining renal function. Secondary hyperparathyroidism would be an unavoidable consequence of aging unless sufficient calcium and/or vitamin D were provided. Since excess PTH removes calcium from bone by stimulating bone resorption, bone mass decreases leading to osteoporosis. In addition, calcium entering soft tissues such as blood vessels and brain, especially the intracellular compartment, may cause functional deterioration of these organs causing hypertension, arteriosclerosis and senile dementia.

The kidney and vasculature are rich sources of NADPH oxidase–derived ROS, which under pathological conditions play an important role in renal dysfunction and vascular damage. Strong experimental evidence indicates that increased oxidative stress and associated oxidative damage are mediators of renovascular injury in cardiovascular pathologies. Increased production of superoxide anion and hydrogen peroxide, reduced nitric oxide synthesis, and decreased bioavailability of antioxidants have been demonstrated in experimental and human hypertension.