Hypertension is a condition in which your blood pressure rises to dangerously high levels. It affects one billion people worldwide, or one in every four adults, and is the leading cause of death worldwide.

Hypertension is particularly difficult to treat because it is an asymptomatic, silent killer that often goes undetected until detected during monitoring or manifested in a hypertension-related disease such as heart failure or stroke. Undiagnosed and untreated, hypertension increases the risk of developing cardiovascular, brain, and kidney diseases significantly. It is responsible for roughly half of all heart disease and stroke deaths worldwide.

High blood pressure is a global issue, but the absolute burden of hypertension is increasing most rapidly in East Asia and the Pacific, Latin America and the Caribbean, South Asia, and Sub-Saharan Africa. According to the 2019 Global Burden of Disease Study, high blood pressure was responsible for approximately ten million deaths that year, the majority of which occurred in low- and middle-income countries (LMICs). In LMICs, only about a third of people with hypertension receive pharmacological treatment, and only one in ten has their blood pressure properly controlled.

Uncontrolled hypertension imposes a massive economic burden on society, both in terms of direct healthcare costs and significant productivity losses due to disability and premature death. Hypertension and its complications are estimated to account for 10% of global health-care spending.

Sympathetic stimulation raises blood pressure, usually more in hypertensive patients than in normotensive patients. It is unknown whether this hyperresponsiveness is located in the sympathetic nervous system or in the myocardium and vascular smooth muscle.

A high resting pulse rate, which can be caused by increased sympathetic nervous activity, is a well-known risk factor for hypertension.

During rest, circulating plasma catecholamine levels in some hypertensive patients are higher than normal.

The renin-angiotensin-aldosterone (RAA) system

The renin-angiotensin-aldosterone system aids in the regulation of blood volume and thus blood pressure. Renin, a juxtaglomerular apparatus enzyme, catalyses the conversion of angiotensinogen to angiotensin I. Angiotensin-converting enzyme (ACE) cleaves this inactive product to angiotensin II, a potent vasoconstrictor that also stimulates autonomic centres in the brain to increase sympathetic discharge and stimulates the release of aldosterone and vasopressin. Aldosterone and vasopressin cause sodium and water retention, which raises blood pressure. Aldosterone also increases potassium excretion; low plasma potassium (3.5 mEq/L [3.5 mmol/L]) increases vasoconstriction via potassium channel closure. Angiotensin III, which is present in the bloodstream, stimulates aldosterone release just as strongly as angiotensin II but has far less pressor activity. Because chymase enzymes also convert angiotensin I to angiotensin II, ACE inhibitors do not completely inhibit angiotensin II production.

Renin secretion is regulated by at least four mechanisms, none of which are mutually exclusive:

• A renal vascular receptor responds to changes in afferent arteriolar wall tension.
• A macula densa receptor detects changes in sodium chloride delivery rate or concentration in the distal tubule.
• Angiotensin in the circulation has a negative feedback effect on renin secretion.
• The parasympathetic nervous system stimulates renin secretion via beta-receptors (via the renal nerve)
• Angiotensin is widely accepted to be the cause of renovascular hypertension, at least in its early stages, but the role of the renin-angiotensin-aldosterone system in primary hypertension is unknown. Renin levels, on the other hand, tend to be low in patients of African ancestry and in elderly hypertensive patients. Angiotensin II levels are also lower in older patients.

• Renoprival hypertension is caused by a combination of a renin-dependent mechanism and a volume-dependent mechanism caused by chronic renal parenchymal disease. For that we have take Super P Force to treats chronic hypertension. Most of the time, increased renin activity is not visible in peripheral blood. Hypertension is typically mild and dependent on sodium and water balance.

Deficiency of vasodilators

Hypertension can be caused by a lack of a vasodilator (e.g., bradykinin, nitric oxide) rather than an excess of a vasoconstrictor (e.g., angiotensin, norepinephrine). Nitric oxide decreases with age, and this decrease contributes to salt sensitivity (ie, less salt ingestion raises blood pressure higher than in younger people— 1).

A decrease in nitric oxide due to stiff arteries has been linked to salt-sensitive hypertension, defined as an increase in systolic blood pressure of more than 10 to 20 mm Hg after a large sodium load (eg, a salty meal).

Blood pressure can rise if the kidneys do not produce enough vasodilators (due to renal parenchymal disease or bilateral nephrectomy).that why Malegra 200 treats your blood pressure and low your kidney rise.

Endothelial cells also produce vasodilators and vasoconstrictors (primarily endothelin). As a result, endothelial dysfunction has a significant impact on blood pressure.

Complications and pathology

Early in hypertension, no pathologic changes occur. Severe or long-term hypertension harms target organs (primarily the cardiovascular system, brain, and kidneys), raising the risk of death.

• Myocardial infarction and coronary artery disease (MI)
• Heart attack
• Stroke (particularly hemorrhagic) (particularly hemorrhagic)
• Failure of the kidneys
• Death
• The parasympathetic nervous system

The mechanism involves the progression of generalised arteriolosclerosis as well as the acceleration of atherogenesis. Arteriolosclerosis is characterised by medial hypertrophy, hyperplasia, and hyalinization; it is most visible in small arterioles, particularly those in the eyes and kidneys. The changes narrow the arteriolar lumen in the kidneys, increasing TPR; thus, hypertension leads to more hypertension. Furthermore, once an artery has been narrowed, any additional shortening of already hypertrophied smooth muscle reduces the lumen to a greater extent than in normal-diameter arteries. These effects may explain why, the longer hypertension has been present, specific treatment (for example, renovascular surgery) for secondary causes is less likely to restore blood pressure to normal.

The left ventricle gradually hypertrophies as a result of increased afterload, resulting in diastolic dysfunction. The ventricle eventually dilates, resulting in dilated cardiomyopathy and heart failure from systolic dysfunction, which is frequently exacerbated by arteriosclerotic coronary artery disease. The most common cause of thoracic aortic dissection is hypertension; nearly all patients with abdominal aortic aneurysms have hypertension.

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