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(From Wikipedia, the free encyclopedia)

Hypertension, also referred to as high blood pressure, HTN or HPN, is a medical condition in which the blood pressure is chronically elevated.

Hypertension can be classified as either essential (primary) or secondary. Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition. About 95% of hypertension is essential hypertension. Secondary hypertension indicates that the high blood pressure is a result of (i.e., secondary to) another condition, such as kidney disease or tumours (adrenal adenoma or pheochromocytoma).

Persistent hypertension is one of the risk factors for strokes, heart attacks, heart failure and arterial aneurysm, and is a leading cause of chronic renal failure. Even moderate elevation of arterial blood pressure leads to shortened life expectancy. At severely high pressures, defined as mean arterial pressures 50% or more above average, a person can expect to live no more than a few years unless appropriately treated. Beginning at a systolic pressure of 115 mm Hg and diastolic pressure of 75 mm Hg (commonly written as 115/75 mm Hg), cardiovascular disease (CVD) risk doubles for each increment of 20/10 mm Hg.


In individuals older than 50 years, hypertension is considered to be present when a person's blood pressure is consistently at least 140 mm Hg systolic or 90 mm Hg diastolic. Patients with blood pressures over - 130/80 mm Hg along with Type 1 or Type 2 diabetes, or kidney disease require further treatment.

Resistant hypertension is defined as the failure to reduce BP to the appropriate level after taking a three-drug regimen. Guidelines for treating resistant hypertension have been published in the UK, and US.

In the United States, prehypertension is defined as blood pressure from 121/81 mm Hg to 139/89 mm Hg and although not a disease category, it is a designation chosen to identify individuals at high risk of developing hypertension.


Essential (primary) hypertension

By definition, essential hypertension has no identifiable cause. However, several risk factors have been identified, including obesity, salt sensitivity, renin homeostasis, insulin resistance, genetics, and age.


The risk of hypertension is 5 times higher in the obese as compared to those of normal weight and up to two-thirds of cases can be attributed to excess weight. More than 85% of cases occur in those with a Body mass index greater than 25. A definitive link between obesity and hypertension has been found using animal and clinical studies, from these it has been realized that many mechanisms are potential causes of obesity induced hypertension. These mechanisms include the activation of the sympathetic nervous system as well as the activation of the renin–angiotensin-aldosterone system.

Sodium sensitivity

Sodium is an environmental factor that has received the greatest attention. Approximately one third of the essential hypertensive population is responsive to sodium intake. When sodium intake exceeds the capacity of the body to excrete it through the kidneys, vascular volume expands secondary to movement of fluids into the intra-vascular compartment. This causes the arterial pressure to rise as the cardiac output increases. Local autoregulatory mechanisms counteract this by increasing vascular resistance to maintain normotension in local vascular beds. As arterial pressure increases in response to high NaCl intake, urinary sodium excretion increases and the excretion of salt is maintained at expense of increased vascular pressures. The increased Na+ stimulates ADH and thirst mechanisms, leading to a concentrated urine and the kidneys holding onto water along with the person increasing the intake of water. Also, the water movement between cells and the interstitium plays a minor role compared to this.

The relationship between sodium intake and blood pressure is controversial. Reducing sodium intake does reduce blood pressure, but the magnitude of the effect is insufficient to recommend a general reduction in salt intake.

Role of renin

Renin is an enzyme secreted by the juxtaglomerular apparatus of the kidney and linked with aldosterone in a negative feedback loop. The range of renin activity observed in hypertensive subjects tends to be broader than in normotensive individuals. In consequence, some hypertensive patients have been defined as having low-renin and others as having essential hypertension. Low-renin hypertension is more common in African Americans than white Americans, and may explain why African Americans tend to respond better to diuretic therapy than drugs that interfere with the Renin-angiotensin system.

How high renin levels predispose to hypertension: Increased renin → Increased angiotensin II → Increased vasoconstriction, thirst/ADH and aldosterone → Increased sodium resorption in the kidneys (DCT and CD) → Increased blood pressure.

Some authorities claim that potassium might both prevent and treat hypertension.

Insulin resistance

Insulin is a polypeptide hormone secreted by cells in the islets of Langerhans, which are contained throughout the pancreas. Its main purpose is to regulate the levels of glucose in the body antagonistically with glucagon through negative feedback loops. Insulin also exhibits vasodilatory properties. In normotensive individuals, insulin may stimulate sympathetic activity without elevating mean arterial pressure. However, in more extreme conditions such as that of the metabolic syndrome, the increased sympathetic neural activity may over-ride the vasodilatory effects of insulin. Insulin resistance and/or hyperinsulinemia have been suggested as being responsible for the increased arterial pressure in some patients with hypertension (citation needed). This feature is now widely recognized as part of syndrome X, or the metabolic syndrome.


Hypertension is one of the most common complex disorders.The etiology of hypertension differs widely amongst individuals within a large population.

Hypertension may be secondary to other diseases but over 90% of patients have essential hypertension which is of unknown origin. It is observed though that:

Having a personal family history of hypertension increases the likelihood that an individual develops HPT.(citation needed) Essential hypertension is four times more common in black than white people, accelerates more rapidly and is often more severe with higher mortality in black patients.(citation needed) More than 50 genes have been examined in association studies with hypertension, and the number is constantly growing. One of these gene is angiotensinogen (AGT) gene, studied extensively by Kim et al. They showed that increasing the number of AGT increases the blood pressure and hence this may cause hypertension. Twins have been included in studies measuring ambulatory blood pressure, from these studies it has been suggested that essential hypertension contains a large genetic influence. Supporting data has emerged from animal studies as well as clinical studies in human populations. The majority of these studies support the concept that the inheritance is probably multifactorial or that a number of different genetic defects each have an elevated blood pressure as one of their phenotypic expressions.However, the genetic influence upon hypertension is not fully understood at the moment. It is believed that linking hypertension-related phenotypes with specific variations of the genome may yield definitive evidence of heritability.

Another view is that hypertension can be caused by mutations in single genes, inherited on a mendelian basis.


Hypertension can also be age related, if this is the case it is likely to be multifactorial. One possible mechanism involves a reduction in vascular compliance due to the stiffening of the arteries. This can build up due to isolated systolic hypertension with a widened pulse pressure. A decrease in glomerular filtration rate is related to aging and this results in decreasing efficiency of sodium excretion. The developing of certain diseases such as renal microvascular disease and capillary rarefaction may relate to this decrease in efficiency of sodium excretion. There is experimental evidence that suggests that renal microvascular disease is an important mechanism for inducing salt-sensitive hypertension.

Vitamin D

It has been suggested, as a result of several studies, that vitamin D deficiency is associated with cardiovascular risk factors. It has been observed that individuals with a vitamin D deficiency have higher systolic and diastolic blood pressures than average. Vitamin D inhibits renin secretion and its activity, it therefore acts as a “negative endocrine regulator of the renin-angiotensin system”. Hence a deficiency in vitamin D leads to an increase in renin secretion. This is one possible mechanism of explaining the observed link between hypertension and vitamin D levels in the blood plasma.

Secondary hypertension

Secondary hypertension results from an identifiable cause. With treatment of the underlying cause, secondary hypertension can resolve without the need for anti-hypertensive medications.

Sleep apnea

Sleep apnea is a common, under-recognized cause of hypertension. It is often best treated with nocturnal nasal continuous positive airway pressure, but other approaches include the Mandibular advancement splint (MAS), UPPP, tonsilectomy, adenoidectomy, septoplasty, or weight loss.


Consumption of liquorice (which can be of potent strength in liquorice candy) can lead to a surge in blood pressure. People with hypertension or history of cardio-vascular disease should avoid liquorice raising their blood pressure to risky levels. Frequently, if liquorice is the cause of the high blood pressure, a low blood level of potassium will also be present.

Liquorice extracts are present in many medicines (for example cough syrups, throat lozenges and peptic ulcer treatments).


Some renal tumors can cause hypertension. The differential diagnosis of a renal tumor in a young patient with hypertension includes Juxtaglomerular cell tumor, Wilms' tumor, and renal cell carcinoma, all of which may produce renin. The tumor pheochromocytoma (most often located in the adrenal medulla) increases secretion of catecholamines such as epinephrine and norepinephrine, causing excessive stimulation of adrenergic receptors, which results in peripheral vasoconstriction and cardiac stimulation. This diagnosis is confirmed by demonstrating increased urinary excretion of epinephrine and norepinephrine and/or their metabolites (vanillylmandelic acid).

Renal hypertension

Hypertension produced by diseases of the kidney. This includes diseases such as polycystic kidney disease or chronic glomerulonephritis. Hypertension can also be produced by diseases of the renal arteries supplying the kidney. This is known as renovascular hypertension; it is thought that decreased perfusion of renal tissue due to stenosis of a main or branch renal artery activates the renin-angiotensin system.

Adrenal hypertension

Hypertension is a feature of a variety of adrenal cortical abnormalities. In primary aldosteronism there is a clear relationship between the aldosterone-induced sodium retention and the hypertension.

Cushing's syndrome

Cushing's syndrome is a condition where both adrenal glands can overproduce the hormone cortisol. Hypertension results from the interplay of several pathophysiological mechanisms regulating plasma volume, peripheral vascular resistance and cardiac output, all of which may be increased. More than 80% of patients with Cushing's syndrome have hypertension.

Coarctation of the aorta

The congenital abnormality aortic coarctation can result in hypertension.


Certain medications, especially NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Licorice (Glycyrrhiza glabra) inhibits the 11-hydroxysteroid hydrogenase enzyme (catalyzes the reaction of cortisol to cortisone) which allows cortisol to stimulate the Mineralocorticoid receptor (MR) which will lead to effects similar to hyperaldosteronism, which itself is a cause of hypertension.

Rebound hypertension

High blood pressure that is associated with the sudden withdrawal of various antihypertensive medications is called Rebound Hypertension. The increases in blood pressure may result in blood pressures greater than when the medication was initiated. Depending on the severity of the increase in blood pressure, rebound hypertension may result in a hypertensive emergency. Rebound hypertension is avoided by gradually reducing the dose (also known as "dose tapering"), thereby giving the body enough time to adjust to reduction in dose.

Medications commonly associated with rebound hypertension include centrally-acting antihypertensive agents, such as clonidine and beta-blockers.



Most of the mechanisms associated with secondary hypertension are generally fully understood. However, those associated with essential (primary) hypertension are far less understood. What is known is that cardiac output is raised early in the disease course, with total peripheral resistance (TPR) normal; over time cardiac output drops to normal levels but TPR is increased. Three theories have been proposed to explain this:

Inability of the kidneys to excrete sodium, resulting in natriuretic factors such as Atrial Natriuretic Factor being secreted to promote salt excretion with the side-effect of raising total peripheral resistance. An overactive Renin-angiotensin system leads to vasoconstriction and retention of sodium and water. The increase in blood volume leads to hypertension. An overactive sympathetic nervous system, leading to increased stress responses. It is also known that hypertension is highly heritable and polygenic (caused by more than one gene) and a few candidate genes have been postulated in the etiology of this condition.


The degree to which hypertension can be prevented depends on a number of features including: current blood pressure level, changes in end/target organs (retina, kidney, heart - among others), risk factors for cardiovascular diseases and the age at presentation. Unless the presenting patient has very severe hypertension, there should be a relatively prolonged assessment period within which should be repeated measurements of blood pressure. Following this, lifestyle advice and non-pharmacological options should be offered to the patient, before any initiation of drug therapy.

The process of managing hypertension according the guidelines of the British Hypertension Society suggest that non-pharmacological options should be explored in all patients who are hypertensive or pre-hypertensive. These measures include;

  • Weight reduction and regular aerobic exercise (e.g., walking) are recommended as the first steps in treating mild to moderate hypertension. Regular exercise improves blood flow and helps to reduce resting heart rate and blood pressure. Several studies indicate that low intensity exercise may be more effective in lowering blood pressure than higher intensity exercise. These steps are highly effective in reducing blood pressure, although drug therapy is still necessary for many patients with moderate or severe hypertension to bring their blood pressure down to a safe level.

  • Reducing dietary sugar intake

  • Reducing sodium (salt) in the diet may be effective: It decreases blood pressure in about 33% of people (see above). Many people use a salt substitute to reduce their salt intake.

  • Additional dietary changes beneficial to reducing blood pressure includes the DASH diet (dietary approaches to stop hypertension), which is rich in fruits and vegetables and low-fat or fat-free dairy foods. This diet has been shown to be effective based on research sponsored by the National Heart, Lung, and Blood Institute. In addition, an increase in daily calcium intake has the benefit of increasing dietary potassium, which theoretically can offset the effect of sodium and act on the kidney to decrease blood pressure. This has also been shown to be highly effective in reducing blood pressure.

  • Discontinuing tobacco use and alcohol consumption has been shown to lower blood pressure. The exact mechanisms are not fully understood, but blood pressure (especially systolic) always transiently increases following alcohol or nicotine consumption. Besides, abstention from cigarette smoking is important for people with hypertension because it reduces the risk of many dangerous outcomes of hypertension, such as stroke and heart attack. Note that coffee drinking (caffeine ingestion) also increases blood pressure transiently but does not produce chronic hypertension.

  • Reducing stress, for example with relaxation therapy, such as meditation and other mindbody relaxation techniques, by reducing environmental stress such as high sound levels and over-illumination can be an additional method of ameliorating hypertension. Jacobson's Progressive Muscle Relaxation and biofeedback are also used, particularly, device-guided paced breathing, although meta-analysis suggests it is not effective unless combined with other relaxation techniques.

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