Vascular Reactivity in Hypertension

Vascular Re act in HypertensionVascular Reactivity in HypertensionIntroductionHigh air obligate ( high tide rip embrace) is oneness of the most burning(prenominal) preventable puddles of morbidity and premature death in the world. The study risk factor for ischemic and myocardial infarction, tenderheartedness failure, chronic nephritic failure, premature death, cognitive decline and hemorrhagic stroke is hypertention. Untreated hypertension is usually associated with a progressive increase of business pressure. Vascular and kidney it can cause lead to a was resistant to treatmentBlood pressure is everydayly distributed in the population and not cut from the natural point above which hypertension is certainly and below which it is not. The associated risk with the increase in race pressure is continuously, with each increase of 2 mmHg in systolic blood pressure associated with an increase risk of 7% of deaths from ischemic heart disease and 10% change magnitude risk of s troke mortality. Hypertension is very common in the UK and prevalence is powerfully influenced by age. In any individual, systolic and / or diastolic pressure can be high. Diastolic pressure increases more frequently in younger people 50. With age, systolic hypertension is becoming a bigger problem because of progressive stiffening and loss of performance of large arteries. At least a quarter of adults (And more than half of those over 60) have high blood pressure.Hypertensions clinical management is one of the most common interventions in primary education care, re stick ining about 1 million pounds in just 2006 drug costs.The guideline will accept that prescribers will use a epitome of the drug product characteristics to inform decisions with individual patients.This guide recommends drugs for indications where lose of marketing in the world approval on the date of publication, if in that respect is good say to support this use. Where recommendations were made for the use of drugs outside their approved indications (off label use ), these drugs are marked with a note in the recommendations.What is hypertension?Before accord on hypertension, we must have a clear idea on blood pressure. It is the force exerted on artery walls when the heart pumps blood through the circulatory system. Rhythmic contractions of the left ventricle, results in cyclical changes in blood pressure. During ventricular systole, the heart pumps blood through the circulatory system, and the pressure in the arteries is at its highest aim this is called the systolic blood pressure. During diastole, the blood pressure in the system decreases and the diastolic blood pressure (1).Systolic and mean diastolic pressure during the cardiac speech rhythm is the weighted average blood pressure over time this is called the mean arterial pressure.The alternation of systolic and diastolic creates external and internal motions of the arterial walls, which are sensed as arterial pulsation. Pulse pressure is the difference between systolic and diastolic blood pressure.Blood pressure is regulated byCentral factors the factors that have-to doe with the heartCardiac output.Heart rate.Peripheral factors the factors that affect the blood vesselsDiameter of blood vessels- Blood pressure is inversely proportional to the diam of blood vessels. When the diameter is trim down, the peripheral resistance of elevated blood pressure is increased. Blood vessels, especially arterioles are always in a state partially limited ascribable to vasomotor tone.Blood volumeVenous returnVelocity of blood lightElasticity of blood vesselsPeripheral resistance- Important that keeps this is the diastolic arterial pressure factor. Diastolic pressure is directly proportional to the peripheral resistanceHypertension is high blood pressure. The force of the blood is blood pressure against the walls of arteries as it flows there through. Arteries are blood vessels that carry oxygenated blood from the hea rt to the body tissues.A normal systolic blood pressure less than 140 mm Hg normal diastolic blood pressure less than 90 mmHgPersistent increase in systemic blood pressure is known as hypertension. Clinically, when systolic blood pressure is above 150 mmHg and diastolic blood pressure rises above 90 mmHg, assuming the pressure.(1)Type of hypertensionHypertension has two major types.Primary hypertensionSecondary hypertension,Primary hypertensionPrimary ( native) hypertension is the most common form of hypertension, which represents 90 to 95% of all cases of hypertension. In near all contemporary societies, the increase in blood pressure with age and the risk of becoming hypertensive adults is appreciable. Hypertension results from a complex interaction of genes and environmental factors.Many common with little effect on genetic variations in blood pressure have been identified as well as roughly rare genetic variants with large effects on blood pressure but the genetic basis of hyp ertension is still poorly understood. Several environmental factors influence blood pressure. The lifestyle that lower blood pressure include reducing salt intake in the diet, increased consumption of fruit and low-fat (Dietary Approaches to break dance Hypertension (DASH)) exercise weight loss and reduced alcohol consumption. Stress seems to play a minor role with specific relaxation techniques not back up by the witness. The possible role of other factors much(prenominal) as caffeine, and vitamin D deficiency is less clear. Insulin resistance, which is common in obesity and is a component of Syndrome X (or Metabolic Syndrome), it is also believed to contribute to hypertension. Recent studies have also implicated in early life events (eg, low birth weight, maternal smoking and lack of breastfeeding) as risk factors for essential hypertension adults although the mechanisms linking this adult hypertension remain obscure exhibitions. Essential hypertensionEssential hypertension has a multifactorial aetiologyGenetic factorsBlood pressure tends to run in families and children of hypertensive parents tend to have high blood pressure. Children and parents of the same age with normal blood pressure. foetal factorsSubsequent hypertension pressure associate with low birth weightEnvironmental factorsAmong the many environmental factors that have been proposed, the following seems to be the most importantObesityAlcohol intakeSodium intakeStressHumoral mechanismsThe renin-angiotensin system and the autonomic nervous system, and the natriuretic peptide system, kallikrein-kinin plays a role in the physiologic regulation of short term Changes in blood pressure and have been implicated in the pathogenesis of essential hypertension.Insulin resistanceAn association between diabetes and hypertension has a long syndrome was recognized and described in hyperinsulinemia, glucose intolerance, reduced levels of HDL cholesterol hypertriglyceridemia and central obesity in associati on hypertension.Secondary hypertensionSecondary hypertension is where the elevation of blood pressure is the result of a specific and potentially treatable cause. Secondary forms of hypertension areEndocrine hypertensionThis develops due to hyperactivity of endocrine glands as someConns syndromeCushings syndromeadrenal hyperplasiaNeurogenic hypertensionDisorders of the nervous system that produce hypertension areIncreased intracranial pressureSectioning of nerve fibers from carotid fistulaRenal hypertensionRenal diseases that cause hypertension arediabetic nephropathychronic glomerulonephritischronic tubulointerstitial nephritisHypertension during pregnancyThe arterial blood pressure is increased by the low glomerular filtration rate and retention of sodium and water.Cardiovascular hypertensionThis occurs due to cardiovascular disorders such as,Atherosclerosis harden of blood vesselscoarctation of aorta narrowing of aortaDrugsThere are many medications that cause or aggravate hy pertension.NSAIDs, oralcontraceptives, steroids, carbenoxolone, liquorice, sympathomimetic and vasopressin.Experimental hypertensionHypertension can be produced in practical animals by various methods. Can be produced by,Clamping the renal arteryDenervation of baroreceptors in carotid sinus and aortic archInjections of corticosteroidsInfusion of salts with aldosterone demonstration of hypertensionLeft ventricular failureRenal failureCerebral hemorrhageRetinal hemorrhageTreatments for hypertensionPrimary hypertension can be controlled but not cured. Secondary hypertension but is cured by treatment of hypertension in the cause of disease. Different types of antihypertensive drugs are given.Diuretics stir diuresis and reduce the volume of extracellular fluid and blood. So blood pressure is decreasedVasodilators Cause vasodilation reducing the blood pressure.Inhibitors of angiotensin converting enzyme Blood pressure is reduced due to formation of angiotensin is blocked.Beta blockers Be ta blockers block the sympathetic beta receptors. Thus, cardiac output is reduced. Inhibits vasoconstriction leading to drop in blood pressure.calcium channel blockers Calcium channel in the myocardium are blocked by these drugs reduce myocardial contractility. Cardiac output to the drop in blood pressure is reduced (3).What is the vascular responsiveness?Vascular reactivity is essential in vascular function that allows the circulatory system to respond to physiological and pharmacological stimuli which pick out adjustment of blood flow and the vascular tone and diameter. Vascular reactivity occurs in two modes. Reactivity are vasoconstrictor and vasodilator reactivity. These forms may be exposed to levels both microvascular and macrovascular.Vascular reactivity in hypertensionVascular reactivity in humans has been studied in many different conditions with a variety of methods. The most effective methods use either intra-arterial or intravenous infusion after inhibition of sympathe tic outflow and interpret the changes in flow and pressure in terms of work instead of vasoconstriction of resistance.Using these methods, the vascular reactivity to various substances, including norepinephrine and angiotensin II has been found to be increased in essential hypertension, but not in various types of renal hypertension.Some studies have shown that alpha-methyldopa, guanethidine and increased vascular reactivity, although lower blood pressure. Glucocorticoids increase reactivity in normotensive subjects, but not in patients with essential hypertension. Aldosterone and salt increased vascular reactivity, especially in hypertensive patients, but slightly in normotensive individuals (2).Vascular reactivity to different vasopressors has been extensively studied in different types of hypertension in experimental animals. The mechanisms underlying this hyper-responsiveness and its role in the ontogeny of hypertension are unclear. But, it has been suggested that high blood pr essure may induce morphological changes in the vessel wall adaptation, resulting in an increase of the wall lm ratio. This could responsible for the increase in vascular reactivity vasoconstrictors stimuli (4).Increased vascular reactivity in hypertension occurs in response to a variety of vasoconstrictor agents, epinephrine, norepinephrine, posterior pituitary extracts, tyramine and renin.Exposure to focus increases sympathetic outflow, and vasoconstriction induced stress can lead to vascular hypertrophy, which leads to progressive increases in peripheral resistance and blood pressure is repeated. People with a family history of hypertension and sympathetic vasoconstrictor obvious stressors increased laboratory tests such as cold and mental stress responses(5).Vascular reactivity to endothelin in hypertensive patientsEndothelin is a potent vasoconstrictor substance as produced by the cardiovascular system. Therefore, a pathophysiological role of this peptide has been proposed und er these conditions, such as hypertension, characterized by the increased vascular tone. The vasoconstrictor response to endothelin-1 is slightly higher in hypertensive patients than in normal subjects.There is an increase of the activity of the vascular endothelin in patients with essential hypertension, which may be the pathophysiological relevance to their increased vascular tone (6).Vascular reactivity to catecholamine in hypertensive patientsIn genetic essential hypertension, vascular reactivity is increased to vasoactive substances which act on the vascular sympathetic neuronal receptor complex and. Since this increase in reactivity is present in early disease progression and even pre-essential hypertension and associated with certain abnormal metabolism of catecholamines, this is probably an etiological factor. Inherited hypertension is probably caused by an abnormal gene or genes produce an abnormal protein or proteins that directly or indirectly affect sympathetic neural a nd systemic vascular contracted receptor sites (7).Established in human hypertension, baroreceptor mechanisms remain active. But the blood pressure is maintained at a high level again in place of the normal blood pressure. This process is known as reset baroreceptor. The upward adjustment of these baroreceptors occurs not only in the primary or essential hypertension, high blood pressure, but also secondary to renal disease or other types. In most patients with open hypertension, catecholamine excretion is within normal limits so that if the neurological part kept the blood pressure is increased in pressure, is probably the result of an increased effect activity nerve quite a than an increase in the activity itself. This could occur by an increase in the sensitivity of the blood vessels to the endogenous norepinephrine produced by the sympathetic nerve endings.The hypertensive patients have a significantly greater response to norepinephrine than normal subjects. There are a numb er of possible relationships between increased vascular reactivity and high blood pressure. An important preliminary to elucidating the significance of the altered vascular reactivity is to determine whether it represents a metabolic or a structural vascular abnormality, which causes high blood pressure, or whether it is one of the ways in which a rise in blood pressure, initiated by some other mechanism, becomes an established change (8). subsequently administrating norepinephrine to the patients with essential hypertension, it has been proven that the initial constriction of vessels is greater in hypertensive individuals than in normotensive individual. Hypertensive patients had a significantly higher response to norepinephrine than normal subjects. There are a number of possible relationships between increased vascular reactivity and high blood pressure. An important preliminary to elucidate the importance of altered vascular reactivity is whether it represents a metabolic abnorm ality or structural vascular, causing high blood pressure, or is one of the means by which an increase in blood pressure he started by another mechanism, becomes a set rate .After the administration of norepinephrine in patients with essential hypertension, it has been shown that constriction of blood vessels is higher than initial hypertensive than in normotensive subjects(9) .ReferencePaul A. Iaizzo. Hand sustain of cardiac anatomy, physiology, and devices. Totowa Humana Press 2005. p. 181-182Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen L. Brooks. Ganongs review of medical physiology. 24th ed. New Delhi McGraw-Hill 2012. p. 590-592Kumar Clark Clinical medicine 6E (857-864)A. E. Doyle, J. R. E. Fraser. Vascular reactivity in hypertension. Journal of the American heart association. 1961 vol 9 755-761Milton Mendlowitz. Vascular reactivity in essential and renal hypertension in man. American heart journal.1967 vol 73. Issue 1 121-128 and Milton Mendlowitz. Vascular reacti vity in systemic arterial hypertension. American heart journal.1973vol 85.issue 2 252-259B. K. Bhattacharya, N. K. Dadkar, A. N. Dohadwalla. Vascular reactivity of perfused vascular bed in spontaneously hypertensive and normotensive rats. Br. J. pharmac.197759243-246 carmine Cardillo, Crescence M. Kilcoyne, Myron Waclawiw, Richard O. Cannon, Julio A. Panza. Role of endothelin in the increased vascular tone of patients with essential hypertension. American heart association.1998.vol 65.James Conway. Vascular reactivity in experimental hypertension careful after hexmethonium. 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