The different forms of angiotensin are denoted by Roman numerals, angiotensin I–IV. The hormones and the way they are activated are often referred to together as the renin–angiotensin system.
The liver creates and releases a protein called angiotensinogen. This is then broken up by renin, an enzyme produced in the kidney, to form angiotensin I. This form of the hormone is not known to have any particular biological function in itself but, is an important precursor for angiotensin II. As it passes in the bloodstream through the lungs and kidneys, it is further metabolised to produce angiotensin II by the action of angiotensin-converting enzyme. Following binding to its receptor, found in most tissues of the body, Angiotensin II has effects on:
The overall effect of angiotensin II is to increase blood pressure, body water and sodium content.
An increase in renin production occurs if there is a decrease in sodium levels and a decrease in blood pressure, which is sensed by the kidneys. In addition, low blood pressure can stimulate the sympathetic nervous system to increase renin production, which results in increased conversion of angiotensinogen to angiotensin I, and so the cylce continues. However, since angiotensin I has to be converted to the more active angiotensin II hormone by the angiotensin-converting enzyme, before it can function, this enables control over angiotensin metabolism. The renin–angiotensin system is also activated by other hormones, including corticosteroids, oestrogen and thyroid hormones. On the other hand, natriuretic peptides (produced in the heart and central nervous system) can impede the renin–angiotensin system in order to increase sodium loss in the urine.
Too much angiotensin II is a common problem resulting in excess fluid being retained by the body and, ultimately, raised blood pressure. This often occurs in heart failure where angiotensin is also thought to contribute to growth in the size of the heart. To combat these adverse effects, drugs such as angiotensin-converting enzyme inhibitors and angiotensin receptor blockers are used in the clinic, although these do have side effects and can lead to excessive retention of potassium (hyperkalaemia).
Control of plasma sodium and potassium concentrations, and the regulation of blood volume and pressure, are all hormonal mechanisms that are impaired by low angiotensin levels. Absence of angiotensin can be associated with retention of potassium, loss of sodium, decreased fluid retention (increased urine output) and low blood pressure.
Last reviewed: Dec 2016