A rterial hypertension in diabetes mellitus

It is known that angiotensin I under the action of dipeptidylcarboxypeptidase, or ACE, is converted into the active octapeptide – angiotensin II. By binding to specific receptors on cell membranes, angiotensin II mediates the main cardiovascular effects, causing an increase in cardiac output, vasoconstriction of the coronary arteries, hyperplasia and hypertrophy of smooth muscle cells, and promotes the release of catecholamines. In recent years, it has been shown that the main components of this system (renin, angiotensinogen, ACE) can be synthesized in the heart, brain, and other organs and tissues.

The following variants of localization of ACE in tissues can be noted:

1) in the endothelium of the blood vessels of the lung, brain, vascular peripheral bed, where the local formation of peptides (ATII and bradykinin) helps to maintain the tone of resistive vessels;

2) in cardiac tissue, where ACE as a factor of the local renin-angiotensin system is involved in the regulation of myocardial contractile function, the growth of cardiomyocytes and the development of cardiac hypertrophy;

3) in serum, where the activity of ACE is relatively small, and is supported by the release from tissues (primarily from the lungs) and serves to generalize the formation of ATII. ACE is also found in mononuclear cells, T lymphocytes and fibroblasts;

4) in epithelial cells, such as the ciliary border of the kidneys, placenta, intestines, etc., involved in adsorption and transport processes;

5) the ACE localization is diverse in the brain tissues: in the endothelium of the brain vessels, bodies and axons of the nerve cells;

6) the highest ACE activity was detected in the seminal fluid and reproductive organs. In microvessels, ACE is located on cell membranes. Circulating ACE molecules enter the bloodstream, separating from tissue glycoproteins.

In addition, an angiotensin-converting enzyme inactivates bradykinin to inactive metabolites. Bradykinin is one of the stimulators of endothelium secretion of NO, the main endothelial relaxation factor. Thus, ACE is one of the key links in maintaining balance between the factors of vasoconstriction and vasodilatation, and, consequently, the regulation of vascular tone.

Local synthesis of angiotensin II increases under conditions of myocardial overload and as a result of prolonged stretching of the arterial wall due to hypertension. Locally formed angiotensin II acts autocrine as a coronary constrictor. Vascular ACE activity reduces the local ability of the vascular wall to produce the endothelial relaxation factor (NO) by destroying bradykinin.

local_offerevent_note August 26, 2019

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