Angiotensin II in the context of "Oligopeptide"

The renin–angiotensin system (RAS), or renin–angiotensin–aldosterone system (RAAS), is a hormone system that regulates blood pressure, fluid, and electrolyte balance, and systemic vascular resistance.

When renal blood flow is reduced, juxtaglomerular cells in the kidneys convert the precursor prorenin (already present in the blood) into renin and secrete it directly into the circulation. Plasma renin then carries out the conversion of angiotensinogen, released by the liver, to angiotensin I, which has no biological function on its own. Angiotensin I is subsequently converted to the active angiotensin II by the angiotensin-converting enzyme (ACE) found on the surface of vascular endothelial cells, predominantly those of the lungs. Angiotensin II has a short life of about 1 to 2 minutes. Then, it is rapidly degraded into angiotensin III by angiotensinases which are present in red blood cells and vascular beds in many tissues.

Angiotensin-converting enzyme (EC 3.4.15.1), or ACE, is a central component of the renin–angiotensin system (RAS), which controls blood pressure by regulating the volume of fluids in the body. It converts the hormone angiotensin I to the active vasoconstrictor angiotensin II. Therefore, ACE indirectly increases blood pressure by causing blood vessels to constrict. ACE inhibitors are widely used as pharmaceutical drugs for treatment of cardiovascular diseases.

Other lesser known functions of ACE are degradation of bradykinin, substance P and amyloid beta-protein.

Angiotensin-converting-enzyme inhibitors (ACE inhibitors) are a class of medication used primarily for the treatment of high blood pressure and heart failure. This class of medicine works by causing relaxation of blood vessels as well as a decrease in blood volume, which leads to lower blood pressure and decreased oxygen demand from the heart.

ACE inhibitors inhibit the activity of angiotensin-converting enzyme, an important component of the renin–angiotensin system which converts angiotensin I to angiotensin II, and hydrolyses bradykinin. Therefore, ACE inhibitors decrease the formation of angiotensin II, a vasoconstrictor, and increase the level of bradykinin, a peptide vasodilator. This combination is synergistic in lowering blood pressure.

The zona glomerulosa (sometimes, glomerular zone) of the adrenal gland is the most superficial layer of the adrenal cortex, lying directly beneath the renal capsule. Its cells are ovoid and arranged in clusters or arches (glomus is Latin for "ball").

In response to increased potassium levels, renin or decreased blood flow to the kidneys, cells of the zona glomerulosa produce and secrete the mineralocorticoid aldosterone into the blood as part of the renin–angiotensin system. Although sustained production of aldosterone requires persistent calcium entry through low-voltage activated Ca channels, isolated zona glomerulosa cells are considered nonexcitable, with recorded membrane voltages that are too hyperpolarized to permit Ca channels entry. However, mouse zona glomerulosa cells within adrenal slices spontaneously generate membrane potential oscillations of low periodicity; this innate electrical excitability of these cells provides a platform for the production of a recurrent Ca channels signal that can be controlled by angiotensin II and extracellular potassium, the 2 major regulators of aldosterone production. Aldosterone regulates the body's concentration of electrolytes, primarily sodium and potassium, by acting on the distal convoluted tubule of kidney nephrons to: increase sodium reabsorption, increase potassium excretion, increase water reabsorption through osmosis.