What Is an Angiotensin?

Angiotensin is a class of peptides with strong effects of vasoconstriction and stimulation of adrenal cortex secretion of aldosterone, which is involved in the regulation of blood pressure and body fluids. It can be divided into angiotensin -, and is currently studied more in angiotensin , angiotensin , and angiotensin .

Decreased circulating blood volume due to blood loss or decreased renal blood flow due to kidney disease can promote the secretion of renin (an acidic protease) by the juxtaglomerular cells of the juxtaglomerular apparatus. After entering the blood, the blood vessels generated by the liver Angiotensinogen (alpha globulin) is hydrolyzed to angiotensin (10 peptide). When it circulates with the blood through the pulmonary circulation, it is hydrolyzed to angiotensin by peptides, which are partially hydrolyzed by 8 peptides. Angiotensin II is affected by angiotensinase A in plasma and interstitial fluid and is hydrolyzed to angiotensin III of 7 peptide.

Chinese name: Angiotensin

Decomposition process: Angiotensin -
main effect: Participate in the regulation of blood pressure and body fluids

Angiotensin concept

Angiotensin classification

Angiotensin Angiotensin I, Angiotensin II, Angiotensin III.

How angiotensin works

I Angiotensin angiotensin I

Basic Information

Chinese name: angiotensin I

Chinese alias: Angiotensin I;

English name: ANGIOTENSIN I HUMAN ACETATE HYDRATE

English alias: ANGIOTENSIN I ACETATE SALT, HUMAN; ANGIOTENSIN I, HUMAN, SYNTHETIC; Angiotensin I human acetate salt hydrate; Angiotensin I human acetate salt hydrate;

CAS number: 70937-97-2

Molecular formula: C64H95N17O17

Structural formula:

Molecular weight: 1374.54000

Exact mass: 1373.71000

PSA: 539.75000

LogP: 3.85940 ^[1]

II Angiotensin angiotensin II

Basic Information

Chinese name: Angiotensin II;

Chinese alias: human angiotensin II

English name: Angiotensin , human

English alias: Angiotensin II

CAS number: 4474-91-3

Molecular formula: C50H71N13O12

Structural formula:

Molecular weight: 1046.18000

Exact mass: 1045.53000

PSA: 406.34000

LogP: 3.06950 ^[2]

III Angiotensin angiotensin III

Basic Information

Chinese name angiotensin III

English name: ANGIOTENSIN III, HUMAN

English alias: angiotensin I-converting enzyme; ACE INACTIVATOR; ANGIOTENSIN I-CONVERTING ENZYME INACTIVATOR; human AngIII; angiotensin III;

CAS number: 13602-53-4

Molecular formula: C46H66N12O9

Structural formula:

Molecular weight: 931.09100

Exact mass: 930.50800

PSA: 339.94000

LogP: 3.71910 ^[3]

Main role of angiotensin

1. Angiotensin can stimulate the adrenal medulla to secrete adrenaline, and it has no obvious effect of directly contracting blood vessels;

2. Angiotensin can cause systemic arterioles to contract and increase hypertension. In addition, it can also promote the adrenal cortex to secrete aldosterone. Aldosterone acts on the renal tubules to maintain sodium, water and potassium, causing increased blood volume.

3. Through the Na-Ca channel of the cell, the Ca ion concentration increases, causing the blood vessels to contract, thereby increasing the blood pressure (some antihypertensive drugs work by antagonizing the effect); angiotensin III has a weaker vasoconstrictive effect, only blood vessels Angiotensin is 1/5, but the effect of promoting aldosterone secretion is stronger than angiotensin .

Under normal circumstances, because there is very little renin secretion and less angiotensin in the blood, it has no significant effect on blood pressure regulation. However, when there is a major blood loss, due to a significant decrease in arterial blood pressure, renal blood flow is reduced, and angiotensin production is increased, which plays an important role in preventing blood pressure from falling excessively and increasing blood pressure. Patients with chronic renal vasospasm or stenosis, due to reduced renal blood flow and increased angiotensin production, can cause renal hypertension.

Angiotensin Research Overview

Renin is a proteolytic enzyme secreted by the mesangial cells of the juxtaglomerular apparatus. When arterial blood pressure decreases, circulating blood volume decreases, and sympathetic nerves excite, secretion increases (see renin). Renin survives in the blood for about 1 hour. During this period, it catalyzes angiotensinogen in the plasma (synthesized into the plasma by the liver) to continuously produce angiotensin I (10 peptide). Angiotensin I can stimulate the adrenal medulla to release the adrenal glands. Suwa has a weak vasoconstrictive effect. Within a few seconds of the formation of angiotensin I, it is degraded by angiotensin-converting enzymes in the blood and lung tissue to produce angiotensin II (8 peptide), which survives in the blood for about 1 minute and is hydrolyzed by aminopeptidase to Angiotensin III (7 peptide). The latter promotes aldosterone secretion and has a contractile effect on renal blood vessels, which is then inactivated by angiotensinase in the blood and tissues. Angiotensin and are more biologically active, while blood angiotensin concentration is lower. Therefore, the activity of angiotensin is the strongest, which will contract the arterioles and increase the peripheral resistance. It will shrink the veins, increase the amount of blood returned to the heart, increase the ventricular filling pressure, and facilitate the ejection of the heart. It can also promote the reabsorption of sodium and water by teletubular tubules and collecting tubes, and increase the extracellular fluid volume, thereby restoring circulating blood volume. These two effects can increase blood pressure, and in severe blood loss, it can at least increase arterial pressure. To the normal half. It also directly affects the brain, enhances sympathetic vasoconstrictor activity; causes thirst and drinking behavior; and can stimulate the secretion of antidiuretic hormones and adrenocorticotropic hormones. It takes about 20 minutes for renin-angiotensin to take full effect, but it lasts longer. Angiotensinogen and converting enzymes are often present in plasma. The release of renin is a key condition that determines the concentration of angiotensin in plasma. The renin, angiotensin, and aldosterone are a connected system called the renin-angiotensin system or the renin-angiotensin-aldosterone system.

Decreased circulating blood volume due to blood loss or decreased renal blood flow due to kidney disease, etc., can promote the secretion of renin (an acid protease) by the juxtaglomerular cells of the juxtaglomerular apparatus, and after entering the blood, the blood vessels generated by the liver Angiotensinogen (alpha globulin) is hydrolyzed to angiotensin (10 peptide). When it circulates with the blood through the pulmonary circulation, it is hydrolyzed to angiotensin by peptides, which are partially hydrolyzed by 8 peptides. Some blood vessels Angiotensin II is affected by angiotensinase A in plasma and interstitial fluid and is hydrolyzed to angiotensin III of 7 peptide.

Angiotensin can stimulate the adrenal medulla to secrete epinephrine, which has no obvious effect on contracting blood vessels directly; angiotensin can cause systemic arterioles to contract and raise blood pressure. In addition, it can also promote the adrenal cortex to secrete aldosterone. Renal tubules play a role in retaining sodium, water, and potassium, thereby increasing blood volume and increasing blood pressure; angiotensin III has a weaker vasoconstrictive effect, only 1/5 of angiotensin II, but promotes aldosterone secretion But stronger than angiotensin II.

In addition, vasopressin can cause strong contraction of blood vessels, but does not participate in blood pressure regulation under normal circumstances. When the body is in a situation such as blood loss that reduces the circulating blood volume, the concentration of the hormone in the blood will significantly increase, which plays a certain role in maintaining circulating blood volume and maintaining arterial blood pressure.

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Angiotensin experimental data