Regular physical exercise reduces blood pressure. The UK National Health Service advises 150 minutes (2 hours and 30 minutes) of moderate-intensity aerobic activity per week to help prevent hypertension.

It has been suggested 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.

Also, some authorities claim that potassium might both prevent and treat hypertension.

Several classes of antihypertensive agents are recommended, with the choice depending on the cause of the hypertensive crisis, the severity of the elevation in blood pressure, and the usual blood pressure of the person before the hypertensive crisis. In most cases, the administration of intravenous sodium nitroprusside injection which has an almost immediate antihypertensive effect, is suitable (but in many cases not readily available). Besides, nitroprusside runs a risk of cyanide poisoning. Other intravenous agents like nitroglycerine, nicardipine, labetalol, fenoldopam or phentolamine can also be used, but all have a delayed onset of action (by several minutes) compared to sodium nitroprusside.

In addition, non-pharmacological treatment could be considered in cases of resistant malignant hypertension due to end stage kidney failure, such as surgical nephrectomy, laparoscopic nephrectomy, and renal artery embolization in cases of anesthesia risk.

It is also important that the blood pressure is lowered smoothly, not too abruptly. The initial goal in hypertensive emergencies is to reduce the pressure by no more than 25% (within minutes to 1 or 2 hours), and then toward a level of 160/100 mm Hg within a total of 2–6 hours. Excessive reduction in blood pressure can precipitate coronary, cerebral, or renal ischemia and, possibly, infarction.

The diagnosis of a hypertensive emergency is not based solely on an absolute level of blood pressure, but also on the typical blood pressure level of the patient before the hypertensive crisis occurs. Individuals with a history of chronic hypertension may not tolerate a "normal" blood pressure.

In general, individuals with white coat hypertension have lower morbidity than patients with sustained hypertension, but higher morbidity than the clinically normotensive.

However, it should be remembered that all the established published trials on the consequences of high blood pressure and the benefits of treating are based on one-time measurement in clinical settings rather than the generally slightly lower readings obtained from ambulatory recordings.

The debate and conflicting ideas revolve around whether or not it would be feasible to treat white coat hypertension, as there still is no conclusive evidence that a temporary rise in blood pressure during office visits has an adverse effect on health.

In fact, many cross sectional studies have shown that "target-organ damage (as exemplified by left ventricular hypertrophy) is less in white-coat hypertensive patients than in sustained hypertensive patients even after the allowance has been made for differences in clinic pressure". Many believe that patients with "white coat" hypertension do not require even very small doses of antihypertensive therapy as it may result in hypotension, but must still be careful as patients may show signs of vascular changes and may eventually develop hypertension. Even patients with established hypertension that is well-controlled based on home blood pressure monitoring may experience elevated readings during office visits.

The goal of treating systolic hypertension is to delay and reduce the extent of damage to the heart, the cerebrovascular system, and the kidneys. Lifestyle interventions are a crucial element of successful treatment, including a diet low in sodium (salt) and rich in whole grains, fruits, and vegetables. Clinical trials have also documented the beneficial effects of weight loss, increased physical activity, and limiting alcohol consumption.

In addition to lifestyle changes, medication can also be used to reduce systolic hypertension to safe levels, although medications frequently have side effects, often serious.

Although an estimated 50 million or more adult Americans suffer from hypertension, the relative incidence of hypertensive crisis is relatively low (less than 1% annually). Nevertheless, this condition does affect upward of 500,000 Americans each year, and is therefore a significant cause of serious morbidity in the US. About 14% of adults seen in hospital emergency departments in United States have a systolic blood pressure ≥180 mmHg.

As a result of the use of antihypertensives, the rates of hypertensive emergencies has declined from 7% to 1% of people with high blood pressure. The 1–year survival rate has also increased. Before 1950, this survival rate was 20%, but it is now more than 90% with proper medical treatment.

Estimates indicate that approximately 1% to 2% of people with hypertension develop hypertensive crisis at some point in their lifetime. Men are more commonly affected by hypertensive crises than women.

The rates of hypertensive crises has increased and hospital admissions tripled between 1983 and 1990, from 23,000 to 73,000 per year in the United States. The incidence of postoperative hypertensive crisis varies and such variation depends on the population examined. Most studies report and incidence of between 4% to 35%.

Hypertension results from a complex interaction of genes and environmental factors. Numerous common genetic variants with small effects on blood pressure have been identified as well as some rare genetic variants with large effects on blood pressure. Also, genome-wide association studies (GWAS) have identified 35 genetic loci related to blood pressure; 12 of these genetic loci influencing blood pressure were newly found. Sentinel SNP for each new genetic loci identified has shown an association with DNA methylation at multiple nearby Cpg sites. These sentinel SNP are located within genes related to vascular smooth muscle and renal function. DNA methylation might affect in some way linking common genetic variation to multiple phenotypes even though mechanisms underlying these associations are not understood. Single variant test performed in this study for the 35 sentinel SNP (known and new) showed that genetic variants singly or in aggregate contribute to risk of clinical phenotypes related to high blood pressure.

Blood pressure rises with aging and the risk of becoming hypertensive in later life is considerable. Several environmental factors influence blood pressure. High salt intake raises the blood pressure in salt sensitive individuals; lack of exercise, obesity, and depression can play a role in individual cases. The possible role of other factors such as caffeine consumption, and vitamin D deficiency are less clear. Insulin resistance, which is common in obesity and is a component of syndrome X (or the metabolic syndrome), is also thought to contribute to hypertension. One review suggests that sugar may play an important role in hypertension and salt is just an innocent bystander.

Events in early life, such as low birth weight, maternal smoking, and lack of breastfeeding may be risk factors for adult essential hypertension, although the mechanisms linking these exposures to adult hypertension remain unclear. An increased rate of high blood urea has been found in untreated people with hypertensive in comparison with people with normal blood pressure, although it is uncertain whether the former plays a causal role or is subsidiary to poor kidney function. Average blood pressure may be higher in the winter than in the summer.

Secondary hypertension results from an identifiable cause. Kidney disease is the most common secondary cause of hypertension. Hypertension can also be caused by endocrine conditions, such as Cushing's syndrome, hyperthyroidism, hypothyroidism, acromegaly, Conn's syndrome or hyperaldosteronism, renal artery stenosis (from atherosclerosis or fibromuscular dysplasia), hyperparathyroidism, and pheochromocytoma. Other causes of secondary hypertension include obesity, sleep apnea, pregnancy, coarctation of the aorta, excessive eating of liquorice, excessive drinking of alcohol, and certain prescription medicines, herbal remedies, and illegal drugs such as cocaine and methamphetamine. Arsenic exposure through drinking water has been shown to correlate with elevated blood pressure.

Based on these studies, treating to a systolic blood pressure of 140, as long as the diastolic blood pressure is 68 or more, seems safe. Corroborating this, a reanalysis of the SHEP data suggests allowing the diastolic to go below 70 may increase adverse effects.

A meta-analysis of individual patient data from randomized controlled trials found the lowest diastolic blood pressure for which cardiovascular outcomes improve is 85 mm Hg for untreated hypertensives and 80 mm Hg for treated hypertensives. The authors concluded "poor health conditions leading to low blood pressure and an increased risk for death probably explain the J-shaped curve". Interpreting the meta-analysis is difficult, but avoiding a diastolic blood pressure below 68–70 mm Hg seems reasonable because:

- The low value of 85 mm Hg for treated hypertensives in the meta-analysis is higher than the value of 68–70 mm Hg that is suggested by the two major randomized controlled trials of isolated systolic hypertension

- The two largest trials in the meta-analysis, Hypertension Detection and Follow-up Program (HDFP) and Medical Research Council trial in mild hypertension (MRC1) were predominantly middle-aged subjects, all of whom had diastolic hypertension before treatment.

- The independent contributions of diseases and factors other than hypertension versus effects of treatment are not clear in the meta-analysis.

A more contemporary meta-analysis by the Cochrane Hypertension group found no benefits in terms of reduced mortality or morbidity from treating patients to lower diastolic targets than 90–100 mmHg.

Prognosis of individuals with renovascular hypertension is not easy to determine. Those with atherosclerotic renal artery disease have a high risk of mortality, furthermore those who also have renal dysfunction have a higher mortality risk.

However, the majority of renovascular diseases can be improved with surgery.

In terms of treatment for renovascular hypertension surgical revascularization versus medical therapy for atherosclerosis, it is not clear if one option is better than the other according to a 2014 Cochrane review; balloon angioplasty did show a small improvement in blood pressure .

Surgery can include percutaneous surgical revascularization, and also nephrectomy or autotransplantation, and the individual may be given beta-adrenergic blockers. Early therapeutic intervention is important if ischemic nephropathy is to be prevented. Inpatient care is necessary for the management of hypertensive urgencies, quick intervention is required to prevent further damage to the kidneys.

Certain medications, including NSAIDs (Motrin/Ibuprofen) and steroids can cause hypertension. Other medications include extrogens (such as those found in oral contraceptives with high estrogenic activity), certain antidepressants (such as venlafaxine), buspirone, carbamazepine, bromocriptine, clozapine, and cyclosporine.

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 methyl-dopa.

Other herbal or "natural products" which have been associated with hypertension include ma huang, St John's wort, and licorice.

White coat hypertension, more commonly known as white coat syndrome, is a phenomenon in which patients exhibit a blood pressure level above the normal range, in a clinical setting, though they don't exhibit it in other settings. It is believed that the phenomenon is due to anxiety that those afflicted experience during a clinic visit.

The patient's daytime ambulatory blood pressure is used as a reference as it takes into account ordinary levels of daily stress. Many problems have been incurred in the diagnosis and treatment of white coat hypertension.

The term "masked hypertension" can be used to describe the contrasting phenomenon, where a patient's blood pressure is above the normal range during daily living, although it isn't above the normal range when the patient is in a clinic setting.

A treatment plan may involve lactulose, enemas, and use of antibiotics such as rifaximin, neomycin, vancomycin, and the quinolones. Restriction of dietary protein was recommended but this is now refuted by a clinical trial which shows no benefit. Instead, the maintenance of adequate nutrition is now advocated.

The management of ascites needs to be gradual to avoid sudden changes in systemic volume status which can precipitate hepatic encephalopathy, renal failure and death. The management includes salt restriction, diuretics (spironolactone), paracentesis, and transjugular intrahepatic portosystemic shunt.

Few women of childbearing age have high blood pressure, up to 11% develop hypertension of pregnancy. While generally benign, it may herald three complications of pregnancy: pre-eclampsia, HELLP syndrome and eclampsia. Follow-up and control with medication is therefore often necessary.

Exercise hypertension is an excessive rise in blood pressure during exercise. Many of those with exercise hypertension have spikes in systolic pressure to 250 mmHg or greater.

A rise in systolic blood pressure to over 200 mmHg when exercising at 100 W is pathological and a rise in pressure over 220 mmHg needs to be controlled by the appropriate drugs.

Similarly, in healthy individuals the response of the diastolic pressure to 'dynamic' exercise (e.g. walking, running or jogging) of moderate intensity is to remain constant or to fall slightly (due to the improved blood flow), but in some individuals a rise of 10 mmHg or greater is found.

Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.

It is the goal of evolutionary medicine to find treatments for diseases that are informed by the evolutionary history of a disease. It has been suggested that gestational hypertension is linked to insulin resistance during pregnancy. Both the increase in blood sugar that can lead to gestational diabetes and the increase in blood pressure that can lead to gestational hypertension are mechanisms that mean to optimize the amount of nutrients that can be passed from maternal tissue to fetal tissue. It has been suggested that techniques used to combat insulin insensitivity might also prove beneficial to those suffering from gestational hypertension. Measures to avoid insulin resistance include avoiding obesity before pregnancy, minimizing weight gain during pregnancy, eating foods with low glycemic indexes, and exercising.

According to JNC 7, BP goals should be as follows :

- Less than 140/90mm Hg in patients with uncomplicated hypertension

- Less than 130/85mm Hg in patients with diabetes and those with renal disease with less than 1g/24-hour proteinuria

- Less than 125/75mm Hg in patients with renal disease and more than 1 g/24-hour proteinuria

The medical care of patients with hypertensive heart disease falls under 2 categories—

- Treatment of hypertension

- Prevention (and, if present, treatment) of heart failure or other cardiovascular disease

The dual (ET and ET) endothelin receptor antagonist bosentan was approved in 2001. Sitaxentan (Thelin) was approved for use in Canada, Australia, and the European Union, but not in the United States. In 2010, Pfizer withdrew Thelin worldwide because of fatal liver complications. A similar drug, ambrisentan is marketed as Letairis in the U.S. by Gilead Sciences.

Many pathways are involved in the abnormal proliferation and contraction of the smooth muscle cells of the pulmonary arteries in patients with pulmonary arterial hypertension. Three of these pathways are important since they have been targeted with drugs — endothelin receptor antagonists, phosphodiesterase type 5 (PDE-5) inhibitors, and prostacyclin derivatives.

The effects of high blood pressure during pregnancy vary depending on the disorder and other factors. Preeclampsia does not in general increase a woman's risk for developing chronic hypertension or other heart-related problems. Women with normal blood pressure who develop preeclampsia after the 20th week of their first pregnancy, short-term complications--including increased blood pressure--usually go away within about 6 weeks after delivery.

Some women, however, may be more likely to develop high blood pressure or other heart disease later in life. More research is needed to determine the long-term health effects of hypertensive disorders in pregnancy and to develop better methods for identifying, diagnosing, and treating women at risk for these conditions.

Even though high blood pressure and related disorders during pregnancy can be serious, most women with high blood pressure and those who develop preeclampsia have successful pregnancies. Obtaining early and regular prenatal care is the most important thing you can do for you and your baby.

Despite these risks for gestational hypertension, the hemochorial placenta has been favored because of its advantages in the way that it aids in diffusion from mother to fetus later in pregnancy. The bipedal posture that has allowed humans to walk upright has also led to a reduced cardiac output, and it has been suggested that this is what necessitated humans’ aggressive early placental structures. Increased maternal blood pressure can attempt to make up for lower cardiac output, ensuring that the fetus’s growing brain receives enough oxygen and nutrients. The benefits of being able to walk upright and run on land have outweighed the disadvantages that come from bipedalism, including the placental diseases of pregnancy, such as gestational hypertension. Similarly, the advantages of having a large brain size have outweighed the deleterious effects of having a placenta that does not always convert the spiral arteries effectively, leaving humans vulnerable to contracting gestational hypertension. It is speculated that this was not the case with Neanderthals, and that they died out because their cranial capacity increased too much, and their placentae were not equipped to handle the fetal brain development, leading to widespread preeclampsia and maternal and fetal death.

Gestational hypertension in the early stages of pregnancy (trimester 1) has been shown to improve the health of the child both in its first year of life, and its later life. However, when the disease develops later in the pregnancy (subsequent trimesters), or turns into preeclampsia, there begin to be detrimental health effects for the fetus, including low birth-weight. It has been proposed that fetal genes designed to increase the mother’s blood pressure are so beneficial that they outweigh the potential negative effects that can come from preeclampsia. It has also been suggested that gestational hypertension and preeclampsia have remained active traits due to the cultural capacity of humans, and the tendency for midwives or helpers to aid in delivering babies.

Blood pressure control can be accomplished before pregnancy. Medications can control blood pressure. Certain medications may not be ideal for blood pressure control during pregnancy such as angiotensin-converting enzyme (ACE) inhibitors and Angiotensin II (AII) receptor antagonists. Controlling weight gain during pregnancy can help reduce the risk of hypertension during pregnancy.