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Blood and hypertension: the damage of too much pressure .

Primary hypertension (HTN) is predicted to affect one third of the world's population --1.5 billion people--by 2025. (1) HTN increases the risk of developing cardiovascular disease, stroke and renal failure. Untreated HTN poses a significant and increasing burden to the health care system. Between 50 and 80 percent of people with hypertension do not take all their medications. (2)

Successful treatment of HTN relies on comprehensive patient education and ongoing contact with trusted health professionals. It is therefore essential that nurses providing care for those with HTN have a detailed understanding of the physiological events underlying this disease and its outcomes, and of the actions and adverse effects of therapies used in treatment.


One in seven adults in New Zealand, and nearly 50 percent of those over 75 years of age, take medication for hypertension (HTN). (3) Rates of HTN in Maori and Pacific populations are almost twice as high as in other groups. (4)

Worldwide, HTN is the most common contributor to death of any medical risk factor. HTN contributes to the development of heart disease, heart failure, chronic renal failure requiring dialysis, stroke, peripheral vascular disease and cognitive decline. (2) The risk of cardiovascular events doubles for every 20/10mmHg rise in blood pressure above 115/70mmHg. (2) Untreated HTN causes progressive renal and vascular damage, eventually leading to a treatment-resistant state.

Hypertension is usually diagnosed and treated in the community. As this is largely an asymptomatic disease, particularly in its initial stages, compliance with treatment regimes can be problematic, a situation aggravated by adverse effects that may accompany drug therapy. Successful treatment of HTN relies on the patient establishing an ongoing therapeutic relationship with a trusted and knowledgeable health professional. Nurses caring for people with HTN need to understand the underlying rationales for prescribed therapies (including lifestyle interventions) and their possible adverse effects. This enables a better awareness of the impact of various therapies for HTN, leading to more effective support and education during care.


Blood pressure is determined by the rate of blood flow from the heart (cardiac output) and the resistance to that flow provided by the blood vessels (total peripheral resistance or systemic vascular resistance).

In turn, cardiac output (CO) is controlled by the heart rate and the stroke volume--the amount of blood ejected from the ventricle with each contraction (figure 1, p29).

Stroke volume is related to the amount of blood returning to the heart during the diastolic period of the cardiac cycle and the force of contraction pushing blood out of the ventricle during systole. Venous return (or end diastolic volume) is determined by the volume of circulating blood and venous capacitance.

Total peripheral resistance (TPR) is the resistance to flow provided by the blood vessels in the body, particularly the arterioles. Resistance to blood flow varies with alterations to blood vessel diameter, largely controlled by the sympathetic nervous system and hormones.

Blood pressure is maintained within normal range by rapid and medium to long-term mechanisms.

Rapid control

This mechanism corrects changes in blood pressure within seconds, eg when going from lying to a standing position. When a person stands up from lying, blood pools in the lower extremities due to high compliance of the veins. Venous return decreases, causing a drop in stroke volume, cardiac output and thus arterial blood pressure (fig 1).

Baroreceptors are stretch receptors found in the aorta and internal carotid arteries that monitor mean arterial pressure. Decreasing blood pressure leads to a lower firing rate in the baroreceptors. This information is processed by the cardiovascular centres in the brainstem.

Responding to low blood pressure created by standing up, baroreceptors increase sympathetic output and decrease parasympathetic output, resulting in (fig 1):

(1) Increased sympathetic nervous action on the heart. Noradrenaline attaches to beta-1 receptors on myocardial cells, leading to:

a) Opening of calcium channels. The increase in calcium coming into the myocardial cells increases the force of contraction, increasing the stroke volume.

b) Increased rate of depolarisation and conduction in the sinoatrial and atrioventricular nodes and purkinje fibres, increasing the heart rate.

(2) Increased sympathetic nervous action on systemic blood vessels.

a) Binding to alpha-1 receptors on veins causes venoconstriction, decreasing venous capacitance so more blood is returned to the heart, increasing stroke volume.

b) Binding to alpha-1 receptors on arterioles, especially in the skin, kidney and gastrointestinal tract, causes vasoconstriction and increased TPR.

(3) Decreased parasympathetic activity reduces the effect of acetylcholine (ACh) on the pacemaker and conduction tissue of the heart. ACh normally hyperpolarises these cells, slowing the heart rate and conduction of action potentials through the heart.

Baroreceptor reflexes cannot regulate blood pressure in the long term, because receptor firing rates adapt to prolonged changes in blood pressure.

Longer-term responses

Within a few minutes of any change to mean arterial pressure (MAP), hormonal mechanisms are activated that act to return pressure to normal over the following hours or days. The key regulatory systems are the renin-angiotensin-aldosterone system (RAAS) and antidiuretic hormone.

Renin-angiotensin-aldosterone system: A decrease in blood pressure causes reduced pressure in the renal arterioles. This, along with sympathetic stimulation (via beta-1 receptors), triggers release of renin from the kidneys. When it is released into the circulation, renin acts upon angiotensinogen, a protein molecule synthesised by the liver. Angiotensinogen is split to create the molecule angiotensin I, which is then converted by angiotensin converting enzyme (ACE) into angiotensin II (figure 2, p31).

Angiotensin II is a potent vasoconstrictor, increasing TPR as an intermediate regulator of blood pressure, reaching peak effect in about 15 to 20 minutes after blood pressure falls. It also exerts several long-term effects through its regulation of sodium and water balance, and thus blood volume (fig 1):

* Increasing sodium reabsorption in the kidney.

* Reducing blood flow through the kidney by causing constriction of the renal arterioles. This decreases glomerular filtrate and urine volume.

* Triggering the secretion of aldosterone from the adrenal cortex that increases sodium reabsorption in the kidney (which takes about 24 hours to reach maximum effect).

The effects of angiotensin II involve binding to the angiotensin II type 1 receptor (AT1R) in target tissues. This receptor may also be involved in the vascular remodelling that occurs in HTN. (7, 8)

Antidiuretic hormone: A decrease in blood pressure acts (via the baroreceptors) on the hypothalamus to increase production of antidiuretic hormone (ADH). If the drop in blood pressure is sudden and severe, ADH can act as a vasoconstrictor. Normally, however, it acts to restore blood pressure by increasing reabsorption of water from the collecting ducts of the kidneys, increasing blood volume. (9)

These short and long-term mechanisms maintain blood pressure on a minute-by-minute and day-today basis--maintaining adequate oxygen and nutrient flow to our tissues and removal of waste--regardless of changes in activity and fluid or sodium intake. They are also the mechanisms activated in the development of HTN, and their unregulated activity can have serious physiological consequences. Drugs used in the treatment of HTN counteract these mechanisms.


Measuring blood pressure gives systolic and diastolic figures: the highest pressure in the artery corresponding to ventricular contraction, and the lowest pressure during relaxation of the left ventricle. HTN is defined as having a blood pressure above 140/90mmHg. This seemingly arbitrary value is determined by a consensus that treating blood pressure above 140/90 will provide more benefit than harm in a population. (10)

The detrimental outcomes of HTN are related to prolonged elevation of mean blood pressure. More recently, the issue of fluctuations in blood pressure has been investigated. A variation in systolic blood pressure over a series of readings is an indicator of increased risk for stroke and other adverse vascular events. Furthermore, some therapies for HTN, eg beta-blockers, may increase blood pressure variability.

Diagnosis of HTN relies on accurate measurement of blood pressure. There is much room for both observer and machine-generated error in measurement (see box, p28). Mercury sphygmomanometers are being phased out of clinical practice, due to health and safety concerns. A common alternative for manual measurement is the anaeroid sphygmomanometer that uses a bellows system, but these may be less accurate. (2)

Automated measurement of blood pressure is increasingly common in many settings, including ambulatory and home self-monitoring. These devices operate by measuring oscillations in cuff pressure as the cuff is deflated. Correct application of the right-sized cuff is important, and accuracy may be lost in the presence of atrial fibrillation or other dysrhythmias. Any type of sphygmomanometer used in clinical practice must be properly validated and maintained, and regularly recalibrated. (2, 11)

Diagnosis of HTN requires at least two measurements of blood pressure, at each of three separate consultations. (11) The New Zealand Cardiovascular Guidelines suggest that home or ambulatory monitoring can be used if there is doubt about the accuracy of clinic measurements, or if HTN is resistant to therapy, or highly variable; however treatment decisions should be based on clinic measurements. (11) More recent guidelines from the United Kingdom (UK)2 say clinic measurement of blood pressure is not superior to ambulatory or home blood-pressure monitoring, and that ambulatory blood-pressure monitoring (ABPM) was superior to either clinic or home monitoring in predicting clinical outcomes of HTN. ABPM can also prevent false positives in HTN diagnosis due to "white coat" HTN (higher than normal blood pressure generated by the presence of clinicians themselves).


The cause of HTN in most individuals is largely unknown. Causative or predisposing factors for primary HTN are hypothesised to include: abnormal sympathetic nervous system activation, genetic variation in sodium reabsorption by the kidney, genetic dysfunction of the renin-angiotensin-aldosterone system, impaired vascular responses, and, in those with diabetes, insulin resistance. (5,6,8,12) These factors all affect TPR, or sodium and water retention, and thus blood volume (fig 1).

Secondary HTN arises as part of another disease process. Examples are chronic renal failure and renal artery stenosis, primary aldosteronism and the use of oral contraceptives. While it is important to eliminate underlying diseases, the majority of people diagnosed with high blood pressure will have primary HTN.


While the underlying cause of primary HTN is unknown, the sequence of events that occur following the onset of HTN are predictable. Vasoconstriction of the systemic arterioles occurs, to produce an increase in TPR. As this continues, the amount of smooth muscle in the walls of the arterioles increases and the blood vessel lining is also thickened to counteract the stress of increased and turbulent blood flow. This leads to permanent narrowing of the arterioles (arteriosclerosis) and thus a permanent rise in TPR, causing treatment-resistant hypertension.

The heart now experiences an increased workload, in that it must pump harder to eject blood into the arterial system against an increased TPR. The cardiac muscle increases in size (cardiac hypertrophy) and this increases the demand for oxygen and nutrients. This may in turn lead to myocardial infarction and left-heart failure.

The coronary arteries respond to increased turbulence with thickening and narrowing of the lumen (arteriosclerosis) and the damage caused by increased, turbulent flow leads to the development of atherosclerotic plaques. The narrowed lumen and plaques reduce flow and lead to decreased oxygen supply to the myocardium, ischaemic heart disease with angina, myocardial infarction and sudden death.

The kidneys also suffer from the effects of vasoconstriction and arteriosclerosis. The decreased blood flow through the kidneys leads to ongoing activation of the RAAS, increased sodium and water retention, increased blood volume and increased blood pressure (fig 1). Decreased blood flow through the kidneys also reduces oxygen supply, leading to hypoxia and necrosis of renal cells and ultimately renal failure.

The aorta and large arteries lose their distensibility; stretch and recoil abilities are reduced, increasing blood pressure further (fig 1). The aortic walls are weakened. This may cause development of dissecting aneurysms.

Atherosclerotic plaques develop in smaller arteries and arterioles as the mechanical stresses of turbulent blood flow cause


After reading this article and completing the associated online learning activities, you should be able to:

* Describe normal physiological mechanisms in the regulation of blood pressure and the way therapies for hypertension impact on these.

* Outline the mechanisms underlying development of primary hypertension and its consequences.

*Discuss pharmacological and other therapies for hypertension.

* Describe common errors in the measurement of blood pressure.

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Measuring BP accurately

Essential to any treatment programme is the accurate assessment of blood pressure so that diagnosis and monitoring are based on correct data. The UK National Institute for Health and Clinical Excellence (NICE) (14) recommends health professionals taking blood pressure recordings have regular reviews of their technique, since errors in diagnosis of HTN frequently occur due to observer error or bias. Some timely reminders of the technical aspects of measurement are given below: (2,11,18)

(1) Allow the patient to rest for a short time before measurement and advise them to avoid exercise, caffeine or smoking prior to the clinic visit. Measurement should determine a resting value, and any of the above factors may give a higher than normal reading. Account should also be taken of the possibility of "white coat" HTN--higher than normal blood pressure generated by the (anxiety-provoking) presence of clinicians themselves.

(2) Ensure tight clothing is removed and the cuff is the correct size. A cuff should cover about 80 percent of the circumference of the arm; too small and the reading will be falsely high, too large and it will give a false low reading. The cuff should be fitted flat and snugly about the arm--a loose cuff will give a falsely high reading. The centre of the cuff should be over the brachial artery.

(3) The systolic pressure should be manually palpated before using the stethoscope. The reason for this is the auscultatory gap that can occur, particularly with HTN. This is where the systolic sounds appear and then disappear briefly before reappearing at a lower level. Failure to ascertain this gap may cause a falsely low systolic pressure recording. To avoid this, the radial or brachial pulse should be palpated while the cuff is inflated to 30mmHg above where it disappears, then note where the pulse reappears on deflation. Deflate the cuff completely and rest the arm briefly before reinflating as the venous engorgement generated by the cuff may give a falsely high diastolic reading.

(4) Normally the diastolic pressure is taken to be at the complete disappearance of sounds. Occasionally there is a muffling of the sounds prior to disappearance. If these are within 10mmHg of each other, the disappearance is recorded as the diastolic value. If the muffling is greater than 10mmHg above disappearance, record both values. If muffling occurs but the sound continues all the way down to zero, take the muffling as the diastolic value.

(5) The cuff should be deflated at a rate of about 2mm per second. If deflated too fast, there may a falsely low systolic or high diastolic reading. Deflate too slowly and venous engorgement will generate a falsely high diastolic pressure.

damage to the linings of the blood vessels. These fatty deposits in the lumen further narrow the vessels and increase TPR even more. Peripheral vascular disease, intermittent claudication, gangrene and arterial leg ulcers can follow. Decreased blood flow to the brain may cause cerebrovascular events such as transient ischaemic attacks, strokes and aneurysms. The eyes too may be affected, with retinal arterial sclerosis.


The goal of treatment in HTN is the reduction of blood pressure to within normal limits. Obviously, the earlier HTN is detected and treated, the less organ damage there will be and the fewer long-term health consequences for the patient.

Treatment and blood pressure targets should be determined by an individual's cardiovascular risk, co-morbidities and age.

The New Zealand Guidelines Group recommends targets of less than 130/80mmHg for most groups, but lower for people with both diabetes and overt renal disease. (11) For mild HTN, moderation of lifestyle may be sufficient to reduce blood pressure, while for moderate or severe HTN, implementing lifestyle changes may reduce the amount of medication required to control blood pressure.

Lifestyle interventions

The focus of lifestyle interventions in HTN is to reduce weight, cholesterol and blood glucose (if elevated) via diet and exercise. Obesity, particularly abdominal obesity, increases the risk of developing HTN by up to 40 percent.


For each 10kg weight loss, there is a drop in systolic blood pressure of 5-20mmHg. (13) Exercising for 30 minutes most days reduces systolic pressure 8mmHg (on average)--probably due to increased weight loss, decreased insulin resistance and decreased cholesterol levels. (14)

Sodium, alcohol and caffeine intakes, and smoking, are all implicated in the development of HTN.

There is ongoing, often media-generated, controversy over salt intake, although experts agree that reducing sodium also reduces blood pressure and adverse cardiovascular outcomes. (15)


For some people, lifestyle modification may be sufficient to reduce blood pressure to within target values. For others, drug therapy, either singly or in combination, may also be indicated. These drug regimes can become quite complex and it is helpful for nurses to have an understanding of the therapies and their common adverse effects, to help with compliance and monitoring.

The common drugs used for treatment of HTN fall into several different classes, all of which act on aspects of the normal short or long-term regulation of blood pressure: sympathetic nervous activation, RAAS activation, and sodium and water retention. Initial therapy usually consists of a thiazide or thiazide-like diuretic, or an angiotensin blocking agent (ACE-inhibitor or ATIR-antagonist), or calcium channel blocker. (2,11) Combinations of these drugs may be necessary as a second step in therapy.


Diuretics treat HTN by increasing sodium and water excretion through the kidneys. This reduces blood volume and venous return, thereby decreasing cardiac output (fig 1).

Thiazide diuretics: Within the thiazide class of diuretics, there are the true thiazides--bendrofluazide and chlorothiazide--and the thiazide-like diuretics--chlorthalidone and indapamide.

Thiazide diuretics act on the renal tubules to inhibit reabsorption of sodium and water. This initial effect of reducing blood volume and thus cardiac output (fig 1) is superseded by a more intricate mechanism with longer use of the drug: thiazides also cause vasodilation, thus reducing TPR. The mechanisms involved are not well understood. (16)

The UK National Institute for Health and Clinical Excellence (NICE) (2) recommends the use of the thiazide-like drugs in preference to older thiazides, because at lower doses they appear to be of more benefit to clinical outcomes.

Because the transport of sodium and potassium are linked in the renal tubules, thiazide diuretics can cause loss of potassium in the urine and consequently hypokalemia. Caution must be taken to monitor for this adverse effect. Thiazides also cause hyperglycaemia, although again, the actual mechanism is not well understood. (16)

Thiazides are excreted in the kidneys using the same transporter that excretes uric acid. Competition for excretion causes increased plasma concentration of uric acid, so thiazides are contraindicated in gout. They may also cause increased cholesterol and male impotence. (17)

Loop diuretics: Furosemide is a more powerful diuretic than the thiazides and acts on the loop of Henle in the kidneys. It generates a large diuresis, again at the expense of plasma potassium and also plasma hydrogen ions. Main unwanted effects are hypokalemia, metabolic alkalosis and hypovolemia. (17)

Spironolactone: This drug acts as a mild diuretic by blocking the action of aldosterone on the kidneys. It acts to increase sodium and water excretion from the kidney, but in the process stimulates reabsorption of potassium, so is referred to as a "potassium-sparing" diuretic. It may cause hyperkalaemia and metabolic acidosis, and a common side-effect is gastro-intestinal upsets. (17)

RAAS inhibition

ACE-inhibitors: Enalapril, captopril, lisinopril and other drugs in this class decrease the formation of angiotensin II. This addresses one of the underlying factors contributing to HTN--unregulated activation of the RAAS. With ACE-inhibition, sodium and water excretion are increased, reducing blood volume, and vasodilation occurs, particularly in the heart, brain and kidney, decreasing TPR (fig 1).

The main unwanted effect of these drugs is hypotension, especially with the first dose and in patients with heart failure where the RAAS is highly activated. Renal artery stenosis is a contraindication for ACE-inhibition: where there is impaired flow into the glomerulus, angiotensin II maintains glomerular filtration pressure by constricting the efferent arteriole. Loss of this mechanism will cause an abrupt loss of renal function. (17)

ACE also breaks down bradykinin. Accumulation of bradykinin with ACE-inhibition is believed to cause development of a persistent dry cough. This is a common adverse effect and is troublesome enough to cause many people to stop taking this class of drugs.

Angiotensin II Type 1 receptor antagonists: Angiotensin II can be formed via alternative enzyme pathways to ACE. Thus, ACE-inhibitors do not block all angiotensin II activity, and the ability to block AT1R has been a step forward in HTN therapy. Losartan and candesartan have similar physiological effects to ACE-inhibitors but without causing a dry cough. (17)

ACE-inhibitors, or AT1R, are the preferred antihypertensive for people with diabetes because they have a renal protective effect. (11) Either class of drugs cause foetal abnormalities and should be used with caution in women of child-bearing age.

Calcium channel blockers

Extracellular calcium is needed for the contraction of both cardiac and vascular smooth muscle. Drugs that block the entry of calcium into these muscle cells reduce the force of contraction and also, in the conduction system of the heart, the rate. These drugs are the most effective in reducing variability in blood pressure. (2)

Calcium channel blockers can be divided into three broad groups: (17)

Acting mainly on myocardium, eg verapamil.

* Acting mainly on vascular smooth muscle, eg nifedipine, felodipine and amlopidine.

* Acting on both myocardium and vascular smooth muscle, eg diltiazem.

The vasodilator effect of these drugs causes a reduction in TPR, but may also induce flushing, headaches and ankle oedema. Verapamil may induce heart block and cause bradycardia. It also causes relaxation of the smooth muscle of the gut, leading to constipation.


Beta-blockers act by preventing noradrenaline binding to its receptors on the cells of the myocardium, airways and peripheral blood vessels. Different drugs in the class act more or less on these targets, depending on whether they are beta-1 specific (eg metoprolol, atenolol), non-specific (eg sotalol, propranolol) or have alpha-receptor activity as well (eg carvedilol, labetalol).

The effect on the heart is to reduce heart rate and contractility, particularly during sympathetic-mediated responses such as exercise and stress. The reduction in cardiac output leads to a decrease in blood pressure. In addition, these drugs decrease the effect of noradrenaline on the RAAS, reducing the release of renin from the kidneys. They may also cause vasodilation of arterioles (mixed alpha and beta blockade) that reduces TPR.

Noradrenaline also causes beta-l-mediated vasodilation, particularly in the skin, skeletal muscle and coronary blood vessels. Beta-blockers prevent this. In the heart, this reduces blood flow to the myocardium, but the impact of reducing heart rate and contractility actually decreases the demand for oxygen in the myocardium, which outweighs the reduction in blood flow. (17) Loss of vasodilation in the muscles and skin can lead to fatigue and cold peripheries in patients being treated with beta-blockers.

The release of noradrenaline leads to bronchodilation via binding to beta-2 receptors. In a healthy person, the loss of this effect when being treated with non-specific beta-blockers has minimal impact, but in the asthmatic this can be serious. Beta-blockers stop the actions of salbutamol and adrenaline on the airways and are therefore not recommended for patients with asthma. (17)

Beta-blockers are not recommended as first-line treatment of hypertension but may be used for pregnant women, in resistant HTN and following myocardial infarction. (11) They are not used in diabetes, due to the effects of beta-blockade on glucose metabolism and that they also mask initial signs of hypoglycaemia (ie tachycardia).

Alpha-1-adrenergic blockers

Stimulation of the alpha-1 receptors by noradrenaline causes constriction of blood vessels and bronchi, relaxation of the gastro-intestinal (GI) tract and contraction of the bladder sphincters. In the circulation, alpha-1 receptors are found mainly in the vessels of the skin, skeletal muscle, kidney and GI tract. Drugs such as prazosin, doxasoxin and terazosin are used to treat hypertension because they induce peripheral vasodilation, leading to a decrease in TPR. They can also cause postural hypotension, impotence, and increased urinary incontinence in women. They may be useful for men with enlarged prostates.



HTN is a largely asymptomatic disease. Treatment is often associated with inconvenience, unpleasant drug side-effects and a need for major lifestyle modification. There are also the associated expenses of doctors' visits for monitoring, ongoing prescription costs and understandable reservations about the effects of long-term drug therapy. (2)

NICE (2) reports that 50 to 80 percent of people with HTN do not take all their medications. Failure to adhere to the medication regime can lead to poorly controlled HTN. Further, erratic compliance can lead to such issues as rebound HTN and organ damage. (2)

Once-daily dosing, and combination pills (eg ACE inhibitor plus thiazide diuretic) increase compliance. Self-monitoring of blood pressure has been shown to have some use in attaining treatment goals, while nurse-led initiatives in lifestyle modification and medication management have also been shown to be effective. (2)


A recent Cochrane review (19) examined the effect of nurse-led clinics in improving management of hypertension. Results were variable but promising and the authors believe there is considerable potential for this type of clinic. The review found that education alone was not sufficient as a management tool for people with hypertension. A multi-faceted approach of education and follow-up, self-monitoring and regular reviews, along with aggressive, protocol-based stepping-up of medication is the most effective course for HTN. (19) The role of nurses working in primary care is expanding to fill this need.

Nurse-led clinics for chronic disease increase client satisfaction and knowledge, improve clinical outcomes and quality of life, and support self-management activities. (20) There are already a number of nurse-led clinics in operation in New Zealand, particularly associated with cardiovascular risk reduction guidelines. (21)


HTN is an asymptomatic disease that can have serious consequences if untreated. The difficulty for people in adhering to a treatment regime is that often the lifestyle changes they are expected to make and the drug regimes they are prescribed, seem complex and difficult, and they may produce side-effects and feelings of ill-health where previously the person had felt perfectly well.

Nurses are ideally situated to provide education and counselling to enable patients to come to terms with their illness, and with the need for ongoing therapy to prevent adverse outcomes in the longer term.


(1) American Society of Hypertension. (2007) Reference list in clinical hypertension, Retrieved 11/8/11.

(2) National Institute for Health and Clinical Excellence (NICE). (2011) Hypertension: The clinical management of primary hypertension in adults. London: National Clinical Guidance Centre.

(3) New Zealand Ministry of Health. (2008) A portrait of health: Key results of the 2006/07 New Zealand Health Survey. Wellington: NZ Ministry of Health, moh.nsf/indexmh/portrait-ofhealth?Open. Retrieved 11/8/11.

(4) National Heart Foundation of Australia. (2010) Guide to management of hypertension 2008 (updated 2010). Clinical-Information/Pages/hypertension.aspx. Retrieved 11/8/11.

(5) Guyenet, P. (2006) The sympathetic control of blood pressure. Nature Reviews: Neuroscience; 7, pp335-346.

(6) Guyton, A. (1991) Blood pressure control--special role of the kidneys and body fluids. Science; 252, ppl813-1816.

(7) Abadir, P. (2011) The frail renin-angiotensin system. Clinics in Geriatric Medicine: 27, pp53-65.

(8) Carey, R. (2011) Overview of endocrine systems in primary hypertension. Endocrinology and Metabolism Clinics of North America: 40, pp265-277.

(9) Singh, M., Mensah, G. & Bakris, G. (2010) Pathogenesis and clinical physiology of hypertension. Cardiology Clinics; 28, pp545-559.

(10) Arguedas, J., Perez, M. & Wright, 1 (2009) Treatment blood pressure targets for hypertension. Cochrane Database of Systemic Reviews; 3:CD004349. 001:10.1002/14651858.CD004349.pub2.

(11) New Zealand Guidelines Group. (2009) New Zealand Cardiovascular Guidelines Handbook: A summary resource for primary care practitioners (2nd ed). Wellington: New Zealand Guidelines Group.

(12) Lastra, G. et al. (2010) Salt, aldosterone and insulin resistance: Impact on the cardiovascular system. Nature Reviews: Cardiology: 7, pp577-584.

(13) Straznicky, N. et al. (2010) European Society Of Hypertension Working Group on Obesity. Antihypertensive effects of weight loss: Myth or reality? Journal of Hypertension; 28:4, pp637-643.

(14) Fagard, R. (2005) Effects of exercise, diet and their combination on blood pressure. Journal of Human Hypertension; 19, S20-S24.

(15) Strazzullo, P. et al. (2009) Salt intake, stroke and cardiovascular disease: Meta-analysis of prospective studies. British Medical Journal; 339, b4567.

(16) Ellison, D. & Loffing, J. (2009) Thiazide effects and adverse effects: Insights from molecular genetics. Hypertension: 54, ppl96-202.

(17) Rang, H. et al. (2007) Rang and Date's Pharmacology (6th ed). Philadelphia PA: Churchill Livingstone Elsevier.

(18) British Hypertension Society. (1999) Blood pressure measurement: Recommendations of the British Hypertension Society (3rd ed). Retrieved 11/8/11.

(19) Glynn, L. et al. (2010) Interventions used to improve control of blood pressure in patients with hypertension. Cochrane Database of Systematic Reviews; 3: CD005182. DOI:10.1002/14651858.CD005182.pub4.

(20) Whitehorse Division of General Practice. (2007) Nurse led clinics. In: Chronic disease management in general practice. Canberra: Australian Government Department of Health and Aging.

(21) Horsburg, M., Goodyear-Smith, F. & Yallop, J. (2008) Nursing initiatives in primary care: An approach to risk reduction for cardiovascular disease and diabetes. New Zealand Family Practitioner; 35:3, ppl76-182.

Georgina Casey, RN, BSc, PGDipSd, MPhil (nursing), is the director of She has an extensive background in nursing education and clinical experience in a wide variety of practice settings.
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Author:Casey, Georgina
Publication:Kai Tiaki: Nursing New Zealand
Geographic Code:8NEWZ
Date:Sep 1, 2011
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