The name renin derives from the Latin "ren" for kidney. It is an enzyme that has a hormone-like effect. Renin is formed in the kidney of vertebrates. The release of renin occurs among other things at low blood pressure.
Catecholamines can also increase renin release. However, key stimuli for the secretion of renin are always associated with a drop in blood pressure. Renin is the initiator of the renin-angiotensin-aldosterone system (RAAS). This serves to increase the blood pressure. Renin was discovered in 1898 by the Finnish physiologist Robert Adolph Armand Tigerstedt.
The enzyme renin consists of two lobes. Between these two lobes lies a gap containing the active site of the enzyme with two catalytic aspartate groups. The inactive precursor of the renin is also known as the prorenin. It is additionally equipped with an N-terminal propeptide. In blood plasma, there is a hundredfold higher concentration of prorenin than of renin.
Renin is an important part of the renin-angiotensin-aldosterone system. The RAAS is a regulated cycle formed by different enzymes and hormones, controlling the water and electrolyte balance in the body. RAAS is one of the most important blood pressure regulating measures of the body.
The renin-angiotensin-aldosterone cascade begins with the release of the enzyme renin. The enzyme is formed in the juxtaglomerular apparatus of the kidney. This consists of specialized connective tissue and blood vessel cells and from the macula densa. In the macula densa are specialized cells of the urinary canals. The juxtaglomerular apparatus has the task to measure the blood pressure in the feeding vessel of the kidney. At the same time it also measures the salinity in the urinary canals and responds to signals and stimuli of the autonomic nervous system. Various hormones also influence the activity of the juxtaglomerular apparatus. When the juxtaglomerular apparatus detects decreased blood flow to the renal corpuscles, more renin is released.
Even if the baroreceptors, the blood pressure sensors of Vas afferens, a reduced blood pressure is measured, renin is released. An increased release of renin is also initiated with a decrease in the amount of fluid in the renal corpuscles. The decrease in the glomerular filtration rate (GFR) also leads to increased secretion as well as a decreased concentration of saline ion in the urine. The salt sensors in the macula densa of the juxtaglomerular apparatus are responsible for the measurement. In summary, renin is released whenever the blood pressure drops and / or when there is a risk of saline and water loss.
Renin acts as a protein-splitting agent and cleaves the hepatic protein angiotensinogen. This is how angiotensin I is transformed into angiotensin II by angiotensin converting enzyme (ACE). Angiotensin II is the end product of the renin-angiotensin-aldosterone cascade. It causes a narrowing of the small blood vessels. This increases the blood pressure. In the adrenal cortex, angiotensin II also causes a release of aldosterone. Aldosterone is a hormone that promotes the reabsorption of water and sodium in the kidney. This mechanism also works to increase blood pressure.
Renin is predominantly produced in the cells of the juxtaglomerular apparatus. The necessary precursors are modified in the endoplasmic reticulum and in the Golgi apparatus of the renin-producing cells after translation. But renin is not only synthesized in the kidneys, but also in some other organs.
The extrarenal production sites of the renin include the uterus, adrenals, pituitary, central nervous system and salivary glands. However, the main production takes place in the kidneys. The renin value is determined in the blood plasma. Normal values are 2.90 - 27.60 pg / ml in adult adults. Normal levels increase to 4.10 - 44.70 pg / ml in standing adults.
An unnaturally high renin value arises, for example, with a low sodium intake, too low blood pressure or a lack of fluids. Also laxatives, diuretics and some hormonal contraceptives increase the renin level in the blood.
In case of overproduction of aldosterone (primary hyperaldosteronism), the renin value may be lowered. Unnaturally low levels occur in patients with diabetes mellitus or with a very high sodium intake.
Renin also plays an important role in the development of high blood pressure (hypertension). In many cases, the high blood pressure is caused by a narrowing of the renal artery, a so-called renal artery stenosis. This stenosis is usually due to arteriosclerosis. In the process, cholesterol degradation products and other substances accumulate in the vessel wall. This thickens, so that the blood in the affected vessels can flow significantly worse. Renal artery stenosis causes renal hypertension. This is triggered by the gold leaf mechanism.
The gold leaf mechanism ensures that kidney renal depletion and thus activation of the renin-angiotensin-aldosterone system occurs when blood flow to the kidney is reduced. By increasing renal water and salt retention and vasoconstriction, blood pressure is increased. This results in arterial hypertension. However, renal hypertension generally develops only when the renal artery is more than 75 percent misplaced.
With a smaller constriction of the renal vessels, the patient may be symptom free. A renin-producing tumor can also lead to hypertension via the activation of RAAS. The same applies to renal cell carcinoma, chronic pyelonephritis, cystic kidney and glomerulonephritis.Tags: