Atherosclerotic Vascular Disease

The preliminary results of comparison of renal artery sympathetic denervation and antihypertensive drugs are quite even. Nevertheless, a prospective, randomized controlled trial of 2014 indicates a different result; after 6 months of closely follow up, there’s no notable antihypertensive effect. Examination of clinical application and building a rigorous indication of intervention should be

Obstruction is the action of obstructing or the state of being obstructed. An obstruction disease is a disease that impedes or prevents passage or progress of blood through the veins or arteries inthe body. Coronary artery disease, also known as atherosclerotic heart disease, is damage or disease to heart's major blood vessels, the arteries. Coronary artery disease is usually caused by a buildup of plaque. This buildup of plaque causes the arteries to become narrow and harder, which limits blood flow to the heart. People that get coronary artery disease can be asymptomatic and not experience any symptoms. But people may experience chest pain, indigestion or nausea, light headness, or sweating, fast heart rate or shortness of breath. CAD has

Angiotensin II (Ang II) is one of the mechanisms that elevates the blood pressure, and is most well known for as being a systemic vasoconstrictor. When Ang II binds to the receptors that are throughout the body, it affects on constricting the blood vessels, which therefore increases the blood pressure. It also has an affect on the kidneys, which increases the sodium retention and hence, altering the process of filtering blood. This then increase the water reabsorption in the kidney, which causes to increase blood volume and also blood pressure (1). Recently, it has been suggested that the role of Ang II may be linked to the physiological and pathological effects to the homeostasis of ER stress of Type 2 Diabetes.

The seriousness of hypertension arises from its impact on a number of organs (target organs). The complications that can develop at their level explain the increased morbidity and mortality associated with hypertension. The heart is one of the main target organs, and one of the first consequences of elevated blood pressure (PA) is left ventricular

The nicotine cause heart diseases; it can destruct the structure and function of your heart and blood vessels. This destruction can lead to Atherosclerosis disease, is a condition in which plaque builds up inside the patient arteries. Atherosclerosis is the dominant predictor of cardiovascular disease as heart failure, arrhythmia and heart valve problems. By time, the plaque limits blood flow and oxygen to the heart, brain and other vital organs, which then cause damage and weakened blood vessels and also can lead to a myocardial infarction, congestive heart failure or arrhythmias, other diseases to the brain as carotid artery disease and can cause kidney diseases. In some cases, if the plague builds

In order to understand the role of ATRAP in humans, it is imperative to understand the role of the AT1 receptor itself. AT1 receptors are crucial elements of the renin-angiotensin system. They act as mediators for almost all physiological roles of angiotensin II (AngII). Inhibiting the binding of angiotensin II to AT1 receptors can effectively lower blood pressure of patients who are found to have hypertension. This observation demonstrates that AT1 receptors, more specifically those found in the kidneys, are important factors in the cause of hypertension in humans (Chen & Coffman, 2015). After understanding regulation model, the function of

Previous studies have shown that there is an association between infection/inflammation and the risk of cardiovascular diseases. This association exists in two patterns: an association between chronic low-grade inflammation/infection and the slow process of atherogenesis, and an association between acute systemic inflammation and a transient increase in the risk of an acute cardiovascular event. It has been suggested that changes in endothelial function may underly the association between inflammation and acute cardiovascular event risk.29 Impaired endothelial function appears to be mediated, at least in part, by systemic inflammation in human vascular disease states. The endothelial dysfunction occurs through a variety of mechanisms such as increased vascular oxidative stress, activation of redox-sensitive transcriptional pathways, and decreased eNOS function. Enhanced formation of reactive oxygen species in vascular wall and reduced endothelial function have all been associated with systemic inflammation.30

causes such as blockage or narrowing of a blood to the kidneys, liver failure causing

Blood pressure is defined as the pressure of blood as it’s applied to the walls of blood vessels when the heart contracts. Blood pressure is important to homeostasis in the body because it helps maintain temperature and proper delivery of nutrients to the body. The kidneys depend on blood pressure for helping it filter blood and they also control one of the mechanisms for regulating blood pressure called long term blood pressure control. When the blood pressure is low, the kidneys release substance/enzyme called renin. Renin causes the production of a chemical known as angiotensin 2 through this cascade of reactions. Then, Angiotensin 2 causes constriction of blood vessels which means the lessening of the diameter in the blood vessels. When blood vessels are constricted the blood pressure rises. Another gland also helps out. This is called the adrenal gland. In this process, the adrenal cortex on the outside of the adrenal gland releases a substance called aldosterone in the presence of angiotensin 2. This substance increases sodium reabsorption in the body. This also increases water reabsorption. In addition, the reabsorbed water increases the blood volume which also increases the

Atherosclerosis is a chronic inflammatory disease characterized by infiltration of blood vessels by lipids and leukocytes. There is a growing body of evidence that among risk factors that promote atherosclerosis, the metabolic syndrome is a powerful and prevalent predictor of cardiovascular events. The systemic inflammatory process associated with the metabolic syndrome has numerous deleterious effects that promote plaque activation, which is responsible for clinical events. Interactions between the innate immune system with lipid?derived products seem to play a major role in the pathophysiology of atherosclerosis in relation with the metabolic syndrome. The multiple links among adipose tissue, the vascular wall, and the immune system are the

Atherosclerosis is a major form of cardiovascular disease which occurs through a processed known as arteriosclerosis in which the arteries become clogged with plaque buildup overtime. Formation of this plaque is due to the damage of endothelial cells (inner cells) that line the walls of arteries. Damage of these cells is triggered by unhealthy practices or other conditions such as smoking, lack of exercise, hypertension, diabetes or high cholesterol levels. As a result harmful material such as fat, cholesterol, palettes and other material deposit themselves into the damaged artery wall. These materials accumulate and form plaque which becomes covered with various cells that try to repair the damaged wall. These cells encapsulate the plaque

The relation of left ventricular mass to salt intake in essential hypertension is well demonstrated in that in such patients 24-h sodium excretion is an independent determinant for relative wall thickness, and is a more powerful determinant than the blood pressure.9,12,13,14 These findings have been confirmed using ambulatory blood pressure monitoring.8 In patients with hypertension associated with type I diabetes multiple regression analysis has identified dietary sodium intake as an independent predictor of left ventricular mass, there was no significant association between left ventricular mass and the blood pressure.15 A high intake of salt increases cardiac mass in both the spontaneous hypertensive rat (SHR) and its control, the Wistar-Kyoto (WKY) rat, though the blood pressure in the WKY rat does not rise.16 In rats with experimental reno-vascular hypertension those on a high intake of sodium have an increase in left ventricular mass which is more consistent than the associated change in blood pressure.17 Though the rise in arterial pressure induced by a high salt diet in the Dahl salt-sensitive rat is prevented by the chronic intracerebroventricular administration of Fab fragments to block brain ouabain this does not prevent the increase in the weight of the left

Large arteries are comprised of three distinct layers. The intima is the endoluminal layer and is lined with endothelial cells bound to a sheet of connective tissue made up predominantly of collagen and proteoglycans. It is in this layer that many of the initial and predominant changes of atherosclerosis occur. The media consists of smooth muscle cells, whereas the adventitia consists mostly of connective tissue elements such as fibroblasts.

In order to distinguish between primary and secondary FSGS, disease presentation and associated medical conditions are very helpful. Suggestive of secondary FSGS are conditions, such as infections, hypertension and obesity, as well as proteinuria that is within nephrotic range, but not accompanied by full blown nephrotic syndrome. Moreover, patients with secondary FSGS will tend to have gradually increasing amounts of protein in the urine. Hence, it is important to find out if the onset of the disease was sudden or subtle with gradual

This plaque formation depends on various factors like if someone have smoking habit, have high blood pressure, have high blood cholesterol level, or have a family history. This blocking of the artery can lead to serious problem including heart attack, stroke or even death. There is also inflammatory response observed by the body to the plaque formation and the conducted by stoll et al showed the results of this inflammatory response.