ANGIOTENSIN (synonym angiotensin) — biologically active octapeptide increasing arterial pressure; in an organism it is formed from α2-глобулина blood under the influence of a renin.
At deficit of sodium in an organism and reduction of blood supply of kidneys in blood it is allocated formed in the juxtaglomerular device renin (see). Being proteinase, he acts on α2-глобулин blood (hypertensinogen), chipping off the decapeptide called by angiotensin I. Under the influence of peptidase from a molecule of physiologically inactive angiotensin I two amino acids (a histidine and a leucine) are chipped off and octapeptide-angiotensin II is formed. The most part of these transformations happens when blood passes through lungs. And. quickly collapses angiotensinases (aminopeptidases, etc.) by eliminating of amino acids from N — the end of a molecule of peptide. Time of half-decay And. 1 — 2 min. Angiotensinases are found in many fabrics, however their most significant amount contains in erythrocytes. Besides, there is a mechanism of capture And. organ vessels.
These biologically active agents interacting among themselves form a renin-angiotenzinnuyu the system which is taking part in regulation of a water salt metabolism and blood circulation.
The amino-acid composition of angiotensin is established by Skeggs (L. T. Skeggs, 1956). The sequence of amino acids in a molecule A. it is established by J. H. Page.
Synthesis identical natural And. it was carried out by Arakawa and Bampes (To. Arakawa. F. M. Bumpus, 1961). And. let's dissolve in water, in ice acetic to - those and ethylene glycol, but it is badly dissolved in alcohol and not dissolved on air, chloroform and amylalcohol; collapses in alkaline condition and in the biological liquids containing angiotensinases; has weak immunological activity.
Physiologically active analogs are synthesized And.: valine-5-angiotensin II, isoleucine-5-angiotensin II, etc. Pressor activity And. depends on availability in its structure of an aromatic ring, a carboxyl group of phenylalanine, phenolic group of tyrosine, availability of proline in the seventh position of a chain of peptide and specific hexapeptide three-dimensional structure.
On force of vasopressor action And. considerably surpasses noradrenaline and, unlike the last, does not cause emission of blood from depot. It is explained by existence sensitive to And. receptors only in precapillary arterioles which are located in an organism unevenly. Therefore action And. on vessels of various areas unequally. The system pressor effect is followed by reduction of a blood-groove in kidneys, intestines and skin and increase it in a brain, heart and adrenal glands. Changes of a blood-groove in muscles are insignificant. Strengthening of cardiac performance is secondary result of change of a hemodynamics, however in experiences on a papillary muscle insignificant direct reinforcing action is shown And. on heart. High doses And. can cause vasoconstriction of heart and brain.
And. affects cardiovascular system and indirectly through a nervous system and closed glands. And. increases secretion of adrenaline and noradrenaline adrenal glands, strengthens vasopressor sympathetic effects and reactions to exogenous noradrenaline. System adrenergic reactions as a result of direct action to nerve centers are described.
Action And. decreases by muscles of intestines as a result of blockade of cholinergic mechanisms atropine and amplifies inhibitors of cholinesterase. Possibly, some so-called reactions mediated through a nervous system on And. are counterregulatory by the nature and result from system or regional changes of blood circulation.
The main cardiovascular reactions on And. result from its direct action on smooth muscles of vessels. Pressor action And. remains after blockade alpha and beta adrenoceptors, after section of vagus nerves, denervation of a carotid sine though the size of reactions can change a little. Pressor action And. amplifies after a bilateral nephrectomy that is caused by elimination of the ternary inhibiting system. One of components of this system — lizofosfolipid — inhibits formation of angiotensin and causes a lowering of arterial pressure.
Influence of a nervous system on education And. in blood it can be carried out through changes of arterial pressure, a tone of vessels of kidneys and, perhaps, as a result of direct nervous influences on secretion of a renin. Adrenergic nerves terminate near cells of the juxtaglomerular device.
And. is to secretagogues Aldosteronum (see). Promoting effect And. on secretion of Aldosteronum it is established by direct experiments with introduction And. in vessels of a perfusing adrenal gland and addition to cuts of adrenal glands.
Stimulation of synthesis of glucocorticoids is insignificant or is absent. Action And. on secretion of Aldosteronum and a water salt metabolism probably action on smooth muscles of vessels is physiologically more important, than, and it is shown in doses, not defiant changes of arterial pressure. In this regard there are bases to consider a renin-angiotenzinnuyu system as renin-angiotensin-aldosteronnuyu system.
And. takes part in regulation of a water salt metabolism, controlling the level of secretion of Aldosteronum and function of kidneys. And. causes reduction of afferent vessels of kidneys, reduction of muscles of a pelvis around direct renal tubules and increase in intra canalicular pressure, reduces a renal blood stream and release of water and sodium. Such reactions are characteristic of the person and some animals (dog). However at rats, rabbits and some other animals And. causes increase in release of water and sodium. Action And. on blood circulation and function of kidneys can change depending on the level of secretion of corticosteroids, water-salt balance, arterial pressure and from a dose of drug. At cirrhosis, severe forms of a circulatory unefficiency with ascites and arterial hypertension And. strengthens a diuresis and release of sodium.
Secretion of a renin and Aldosteronum increases in time orthostatic test (see). Introduction specific to And. antibodies causes temporary hypotension that also demonstrates participation And. in regulation of arterial pressure in physiological conditions. Its physiological properties formed the basis for the assumption of participation And. in a pathogeny of arterial hypertension. However activity of a renin and content of angiotensin in blood of patients with an idiopathic hypertensia are not changed. And. takes part in a pathogeny renal hypertensia, cardiac hypostases and disturbances of a water salt metabolism. At hypotonic states (shock, a collapse) activity of a renin increases more, than activity destroying And. angiotensinases.
And. in blood determine by biological and radio immunological methods [Yu. A. Serebrovskaya, I. A. Uchitel, 1970; Johnston (S. Johnston), 1971).
In clinical practice to treatment of acute hypotonic states (a collapse, traumatic, cardiogenic and hemorrhagic shock, etc.) it is applied Angiotensinamidum (see), synthetic drug from group of angiotenzin.
Synthetic analogs of angiotensin cause cross tachyphylaxis (see), expressed in various degree that, perhaps, is explained by their unequal affinity to receptor system. Ability And. to cause a tachyphylaxis it is rather small, however it can be used as differential and diagnostic test. At renovascular hypertensia introduction And. causes smaller increase in arterial pressure, than at arterial hypertension with normal contents And. in blood. Test has relative value.
Bibliography: Vikhert A. M. and Ushkalov A. F. Various aspects of physiological effect of angiotensin, Cardiology, t. 11, No. 3. page 143, 1971; Krikshtopaytis M. I. Vasoactive polypeptides in clinical practice, Rubbed. arkh., t. 39, No. 12, page 12, 1967, bibliogr.; Liyelays Ya. P. and G. I. Sistem's Chipens a renin — angiotsnzin and its functions in an organism, in book: Chemical and biol. peptides, under the editorship of X. M. Markova, with 113, Riga, 1971, bibliogr.; Markov of X. M. Action of a renin and angiotensin on cardiovascular system, the Stalemate. fiziol. and ekspery. ter., t. 14, No. 4, page 78, 1970, bibliogr.; Markov of X. M and Ivanova I. A. Immunological activity of a renin and angiotensin, Urol. and nefrol., No. 1, page 62, 1971, bibliogr.; Merrifield R. B. Peptide hormones, Recent Progr. Hormone Res., v. 23, p. 451, 1967, bibliogr.; Whelan R. F., Seroop G. S. a. Walsh J. A. Cardiovascular actions of angiotensin in man, Amer. Heart J., v. 77, p. 546, 1969, bibliogr.
A. I. Homazyuk.