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
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
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
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 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
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.
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
Secondary hypertension results from an identifiable cause. With treatment of the
underlying cause, secondary hypertension can resolve without the need for anti-hypertensive
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).
Hypertension produced by diseases of the kidney. This includes diseases such as
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.
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 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.
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
- 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.