Hypertension: What Persistent High Blood Pressure Does to the Body
A patient has their blood pressure checked during a routine appointment. It reads 166/96 mmHg. They look perfectly comfortable, have no headache and are surprised when the nurse repeats it. Yet the result cannot be dismissed simply because they feel well. Hypertension is a sustained rise in arterial blood pressure, and the damage associated with it often develops quietly over years. People may continue with their usual lives while the heart, arteries and kidneys are adapting to that extra pressure.
There are two questions in that clinic room. Is the reading accurate, and does it reflect the pressure this person's circulation experiences most of the time? The answers lead us from the mechanics of taking blood pressure to what happens inside the body when it stays raised.
Where the pressure comes from
During systole, the left ventricle contracts and pushes blood into the aorta. The arterial pressure reaches its peak, giving us the first number. During diastole, the ventricle relaxes and fills, but blood continues flowing through the circulation because elastic arteries recoil and maintain pressure between heartbeats. That is the second number. A reading of 166/96 mmHg tells us the peak and resting arterial pressures are both raised; it does not tell us, on its own, why.
Blood pressure depends partly on cardiac output, the volume the heart pumps each minute, and partly on the resistance offered by the arteries and arterioles. The smaller arteries play a particularly important part because their muscular walls can constrict and relax. When they narrow, it takes more pressure to drive blood through them. The kidneys influence the other side of the equation by controlling how much sodium and water the body retains, and therefore the circulating volume. Nerves and hormones, especially the sympathetic nervous system and renin–angiotensin–aldosterone system, can alter vessel tone and fluid handling. Ageing and stiffening of the larger arteries also change the pressure pattern. Hypertension commonly reflects several of these changes together.
Now look again at the cuff on the patient's arm. A cuff that is too small can produce a falsely high result. An unsupported arm, talking, movement or insufficient rest can also alter the measurement. The nurse checks the cuff size, sits the patient comfortably with their arm supported, and repeats the reading. NICE recommends measuring both arms when considering a diagnosis; if the difference remains greater than 15 mmHg after repeating, subsequent readings are taken from the higher arm. An irregular pulse deserves particular care because some automated devices struggle to measure accurately when the rhythm is irregular, so manual auscultation may be needed.
If the clinic pressure remains between 140/90 and 180/120 mmHg, NICE ordinarily recommends ambulatory blood pressure monitoring (ABPM) to establish whether hypertension is persistent. The monitor records readings as the person goes about an ordinary day. If ABPM is unsuitable or not tolerated, home blood pressure monitoring (HBPM) is an alternative. With home monitoring, readings are taken in pairs morning and evening for at least four days, ideally seven, and the first day's results are excluded from the average. This gives a far better impression of the usual pressure than one appointment.
For most adults, hypertension is confirmed by a clinic pressure of at least 140/90 mmHg together with a daytime ABPM or home average of at least 135/85 mmHg. The different thresholds account for the fact that pressure in a clinical setting does not always represent pressure elsewhere. Some people have substantially higher readings in clinic than at home, often described as a white-coat effect. Others have masked hypertension, where the clinic reading appears acceptable but measurements during everyday life are raised. The danger with the second pattern is that sustained pressure can remain unnoticed if only clinic measurements are considered.
What the arteries, heart and kidneys experience
A higher pressure means that blood is pressing against the arterial walls more forcefully over time. The inner lining, the endothelium, is not an inert coating: it helps regulate vascular tone, inflammation and clotting. Smooth muscle within the vessel wall also responds to the conditions around it. Prolonged hypertension can lead small arteries and arterioles to remodel, with thicker walls and, in some vessels, a narrower lumen. Large arteries may become stiffer. This is not the same as an artery filling up with cholesterol plaque, although hypertension and atherosclerosis often coexist and together increase cardiovascular risk.
The heart faces that increased resistance every time it contracts. To open the aortic valve and eject blood into a circulation with persistently raised pressure, the left ventricle must generate greater force. Over time its muscular wall may thicken, producing left ventricular hypertrophy (LVH). At first, the extra muscle helps the heart work against the load. But thicker myocardium can become less compliant and harder to fill. Pressure may rise behind the left ventricle, through the left atrium and towards the pulmonary circulation, which helps explain why a person with longstanding hypertension can develop breathlessness and heart failure even when the ejection fraction is preserved.
LVH may be suggested by an electrocardiogram (ECG), although a normal ECG does not rule it out. Echocardiography gives a more direct view of ventricular wall thickness and filling. Not everybody with hypertension develops LVH, and other conditions can thicken the heart muscle too. The scan is interpreted with the blood-pressure history and the rest of the clinical picture, rather than treated as proof of one cause.
The kidneys are particularly interesting because they help regulate pressure while also being vulnerable to it. When renal blood flow is perceived as reduced, the kidneys can release renin, triggering a sequence that produces angiotensin II. Angiotensin II constricts blood vessels and stimulates aldosterone release, which encourages sodium retention. Water follows sodium, helping maintain blood volume and pressure. In some forms of hypertension, increased activity in this system contributes to the problem. Its importance also explains why medicines that interrupt angiotensin signalling can lower blood pressure.
Inside the kidneys, blood is filtered through delicate glomerular capillaries. Years of raised pressure can damage the small renal vessels and filtration barrier, allowing albumin, a protein normally kept largely in the bloodstream, to appear in urine. Ongoing damage may reduce kidney function. Once that happens, the kidneys may become less able to manage sodium and water effectively, making blood-pressure control harder still. A urine albumin-to-creatinine ratio (ACR) and blood measurements of creatinine and estimated glomerular filtration rate (eGFR) help reveal changes that a patient may not be able to feel.
The microscopy image shows a form of arteriolar injury that can occur with longstanding hypertension. The vessel wall has become thickened and hyalinised, reducing the space available for blood to pass. Diabetes and other conditions can produce similar appearances, so this is an example of tissue damage, not a test used routinely to diagnose hypertension. Most patients will have urine and blood tests rather than a kidney biopsy.
The same slow injury can affect other organs. Hypertension increases the risk of both ischaemic and haemorrhagic stroke. Damage to small vessels within the brain may accumulate long before a major stroke occurs, and retinal vessels can show characteristic changes when the back of the eye is examined. These consequences help explain why a patient can feel completely well while investigations identify that their circulation has already been under strain.
From investigations to a treatment plan
After confirming persistent hypertension, the team needs to know how much cardiovascular risk is present and whether any organs have been affected. NICE recommends blood tests that include electrolytes, creatinine, eGFR, HbA1c and lipids, together with urine testing for ACR and haematuria, fundal examination and a 12-lead ECG. Each investigation answers a different question. An elevated ACR may suggest kidney damage; a raised HbA1c identifies diabetes that affects vascular risk and treatment; potassium and creatinine provide a baseline before medicines that alter renal salt handling or the renin–angiotensin system are prescribed.
Most hypertension is primary hypertension, with no single identifiable cause. Age, family history, body weight, sodium intake, alcohol, inactivity, sleep disturbance and metabolic factors may contribute in different proportions. A minority of patients have secondary hypertension from a specific condition or substance, such as kidney disease, primary aldosteronism, obstructive sleep apnoea or certain medicines. Unusually early onset, severe or suddenly worsening readings, or blood pressure that remains high despite several medicines can lead to further investigation. Treatment is also influenced by whether the person has diabetes, cardiovascular disease, chronic kidney disease or other risk factors.
For persistent stage 2 hypertension, NICE recommends offering antihypertensive medication alongside lifestyle advice. For stage 1, the decision is more individual: the person's cardiovascular risk, diabetes or kidney disease, existing organ damage, age and preferences all influence the conversation. Lifestyle measures such as reducing excess salt, maintaining activity, managing alcohol intake and stopping smoking can lower risk, but they cannot necessarily undo years of vascular change, and medication is often needed. The purpose of treatment is to reduce the load experienced by the circulation day after day and prevent events that have not yet happened.
Different medicines reduce that load in different ways. ACE inhibitors or angiotensin receptor blockers (ARBs) reduce the effects of the renin–angiotensin system, allowing vessels to relax and sometimes providing additional kidney protection in appropriately selected patients. Calcium-channel blockers, such as amlodipine, relax arterial smooth muscle. Thiazide-like diuretics, such as indapamide, help the kidneys excrete sodium and have longer-term effects on vascular pressure. NICE uses a stepwise selection pathway informed by factors including age, type 2 diabetes and family background, but kidney function, pregnancy possibility, other conditions and tolerability can change the appropriate choice.
There is a practical reason for monitoring after treatment starts. ACE inhibitors and ARBs can raise potassium and cause a change in creatinine; diuretics can disturb sodium or potassium balance and contribute to dehydration; amlodipine may cause ankle swelling. A patient who stopped amlodipine because their shoes no longer fit has not simply 'failed to take their tablets'. That swelling may be the reason treatment has become difficult. Someone taking a diuretic may be avoiding the morning dose because they cannot easily access a toilet at work. Understanding the medicine's effect explains both the expected benefit and the difficulties the person may experience taking it.
Targets are also individualised. Under NICE NG136, the usual clinic target for adults younger than 80 with uncomplicated hypertension is below 140/90 mmHg, while for adults aged 80 and over it is generally below 150/90 mmHg, taking frailty and other conditions into account. Chronic kidney disease with significant albuminuria, for example, may require a different target. A patient whose pressure has fallen into the recommended range but who becomes dizzy on standing still needs review: treatment should lower cardiovascular risk without leaving someone at risk of falling or poor perfusion.
A very high reading changes the immediate assessment. Under NICE guidance, systolic pressure of 180 mmHg or more or diastolic pressure of 120 mmHg or more warrants prompt evaluation for organ damage. If that pressure occurs with new confusion, chest pain, heart-failure symptoms, acute kidney injury, retinal haemorrhage or papilloedema, same-day specialist assessment is required. Stroke symptoms, suspected aortic dissection and acute pulmonary oedema are emergencies. By contrast, someone who is stable and has no symptoms or evidence of acute damage usually needs timely investigation and confirmation rather than an automatic rapid intravenous reduction. When no target-organ damage is found, NICE advises repeat clinic measurement or monitored confirmation with clinical review within seven days.
For the patient whose first reading was 166/96 mmHg, the important outcome may be that home monitoring confirms sustained hypertension, urine and blood results establish whether the kidneys are affected, and a treatment plan is agreed that they can live with. Follow-up then shows whether pressure is falling and whether the treatment is tolerable. Much of hypertension care takes place when the patient feels well. The benefit is often something they never experience: a stroke, heart failure or loss of kidney function that treatment has helped prevent.
References
British Heart Foundation. High blood pressure (hypertension): causes and symptoms. British Heart Foundation.
NHS inform. High blood pressure (hypertension). NHS inform.
British and Irish Hypertension Society (2023) Validated blood pressure monitors.
National Institute for Health and Care Excellence (NICE) (2019, updated 2026) Hypertension in adults: diagnosis and management. NG136. London: NICE.
NHS (2025) High blood pressure.
Unger, T., Borghi, C., Charchar, F. et al. (2020) ‘2020 International Society of Hypertension global hypertension practice guidelines’, Hypertension, 75(6), pp. 1334–1357.