Vascular Reactivity in Hypertension

Posted by on September 28, 2017

Vascular Reactivity in Hypertension Introduction High blood pressure (hypertension) is one of the most important preventable causes of morbidity and premature death in the world. The major risk factor for ischemic and myocardial infarction, heart failure, chronic renal failure, premature death, cognitive decline and hemorrhagic stroke is hypertention. Untreated hypertension is usually associated with a

Vascular Reactivity in Hypertension

Introduction

High blood pressure (hypertension) is one of the most important preventable causes of morbidity and premature death in the world. The major risk factor for ischemic and myocardial infarction, heart failure, chronic renal failure, premature death, cognitive decline and hemorrhagic stroke is hypertention. Untreated hypertension is usually associated with a progressive increase of blood pressure. Vascular and kidney it can cause lead to a was resistant to treatment

Blood pressure is normally 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 blood pressure is continuously, with each increase of 2 mmHg in systolic blood pressure associated with an increased risk of 7% of deaths from ischemic heart disease and 10% increased risk of stroke mortality. Hypertension is very common in the UK and prevalence is strongly 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.

Hypertension’s clinical management is one of the most common interventions in primary education care, representing about 1 million pounds in just 2006 drug costs.

The guideline will accept that prescribers will use a summary of the drug product characteristics to inform decisions with individual patients.

This guide recommends drugs for indications where lack of marketing in the world approval on the date of publication, if there is good evidence 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 understanding 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 level; 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 cycle 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 perceived as arterial pulsation. Pulse pressure is the difference between systolic and diastolic blood pressure.

Blood pressure is regulated by:

Central factors; the factors that affect the heart

  1. Cardiac output.
  2. Heart rate.

Peripheral factors: the factors that affect the blood vessels

  1. Diameter of blood vessels- Blood pressure is inversely proportional to the diameter of blood vessels. When the diameter is reduced, the peripheral resistance of elevated blood pressure is increased. Blood vessels, especially arterioles are always in a state partially limited due to vasomotor tone.
  2. Blood volume
  3. Venous return
  4. Velocity of blood flow
  5. Elasticity of blood vessels
  6. Peripheral resistance- Important that keeps this is the diastolic arterial pressure factor. Diastolic pressure is directly proportional to the peripheral resistance

Hypertension 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 heart to the body tissues.

A normal systolic blood pressure less than 140 mm Hg: normal diastolic blood pressure less than 90 mmHg

Persistent 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 hypertension

Hypertension has two major types.

  1. Primary hypertension
  2. Secondary hypertension,

Primary hypertension

Primary (essential) hypertension is the most common form of hypertension, which represents 90 to 95% of all cases of hypertension. In almost 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 some rare genetic variants with large effects on blood pressure but the genetic basis of hypertension 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 Stop Hypertension (DASH)) exercise weight loss and reduced alcohol consumption. Stress seems to play a minor role with specific relaxation techniques not supported by the witness. The possible role of other factors such 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 hypertension

Essential hypertension has a multifactorial etiology

Genetic factors

Blood 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.

Fetal factors

Subsequent hypertension pressure associate with low birth weight

Environmental factors

Among the many environmental factors that have been proposed, the following seems to be the most important:

  1. Obesity
  2. Alcohol intake
  3. Sodium intake
  4. Stress

Humoral mechanisms

The renin-angiotensin system and the autonomic nervous system, and the natriuretic peptide system, kallikrein-kinin plays a role in the physiological regulation of short term Changes in blood pressure and have been implicated in the pathogenesis of essential hypertension.

Insulin resistance

An 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 association hypertension.

Secondary hypertension

Secondary hypertension is where the elevation of blood pressure is the result of a specific and potentially treatable cause. Secondary forms of hypertension are:

Endocrine hypertension:

This develops due to hyperactivity of endocrine glands as some

  1. Conn’s syndrome
  2. Cushing’s syndrome
  3. adrenal hyperplasia

Neurogenic hypertension:

Disorders of the nervous system that produce hypertension are

  1. Increased intracranial pressure
  2. Sectioning of nerve fibers from carotid sinus

Renal hypertension:

Renal diseases that cause hypertension are

  1. diabetic nephropathy
  2. chronic glomerulonephritis
  3. chronic tubulointerstitial nephritis

Hypertension during pregnancy:

The arterial blood pressure is increased by the low glomerular filtration rate and retention of sodium and water.

Cardiovascular hypertension:

This occurs due to cardiovascular disorders such as,

  1. Atherosclerosis : hardening of blood vessels
  2. coarctation of aorta : narrowing of aorta

Drugs:

There are many medications that cause or aggravate hypertension.

NSAIDs, oralcontraceptives, steroids, carbenoxolone, liquorice, sympathomimetic and vasopressin.

Experimental hypertension

Hypertension can be produced in practical animals by various methods. Can be produced by,

  1. Clamping the renal artery
  2. Denervation of baroreceptors in carotid sinus and aortic arch
  3. Injections of corticosteroids
  4. Infusion of salts with aldosterone

Manifestation of hypertension

  1. Left ventricular failure
  2. Renal failure
  3. Cerebral hemorrhage
  4. Retinal hemorrhage

Treatments for hypertension

Primary 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.

  1. Diuretics: Cause diuresis and reduce the volume of extracellular fluid and blood. So blood pressure is decreased
  2. Vasodilators: Cause vasodilation reducing the blood pressure.
  3. Inhibitors of angiotensin converting enzyme: Blood pressure is reduced due to formation of angiotensin is blocked.
  4. Beta blockers: Beta blockers block the sympathetic beta receptors. Thus, cardiac output is reduced. Inhibits vasoconstriction leading to drop in blood pressure.
  5. 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 reactivity?

Vascular reactivity is essential in vascular function that allows the circulatory system to respond to physiological and pharmacological stimuli which require 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 hypertension

Vascular 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 sympathetic 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 development of hypertension are unclear. But, it has been suggested that high blood pressure may induce structural changes in the vessel wall adaptation, resulting in an increase of the wall: lumen 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 stress 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 patients

Endothelin is a potent vasoconstrictor substance as produced by the cardiovascular system. Therefore, a pathophysiological role of this peptide has been proposed under 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 patients

In hereditary 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 and systemic vascular contractile 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 established 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 rather 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 number 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).

After 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 abnormality 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) .

Reference

  1. Paul A. Iaizzo. Hand book of cardiac anatomy, physiology, and devices. Totowa: Humana Press; 2005. p. 181-182
  2. Kim E. Barrett, Susan M. Barman, Scott Boitano, Heddwen L. Brooks. GanongÂ’s review of medical physiology. 24th ed. New Delhi: McGraw-Hill; 2012. p. 590-592
  3. Kumar & Clark Clinical medicine 6E (857-864)
  4. A. E. Doyle, J. R. E. Fraser. Vascular reactivity in hypertension. Journal of the American heart association. 1961; vol 9: 755-761
  5. Milton Mendlowitz. Vascular reactivity in essential and renal hypertension in man. American heart journal.1967; vol 73. Issue 1: 121-128 and Milton Mendlowitz. Vascular reactivity in systemic arterial hypertension. American heart journal.1973vol 85.issue 2: 252-259
  6. B. K. Bhattacharya, N. K. Dadkar, A. N. Dohadwalla. Vascular reactivity of perfused vascular bed in spontaneously hypertensive and normotensive rats. Br. J. pharmac.1977;59:243-246
  7. 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.
  8. James Conway. Vascular reactivity in experimental hypertension measured after hexmethonium. Journal of the American heart association.1958; 17:807-810

Leave a Reply

Your email address will not be published. Required fields are marked *