Month: August 2019

Vascular damage is manifested as a violation of the endothelial relaxing factor and increased leukocyte adhesion to the epithelium surface. Rheological changes associated with increased adhesiveness of platelets are also of great importance in impaired

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

In recent years, significant progress has been made in studying the genetic factors of hypertension and coronary artery disease. The role of genetic polymorphism in the development of arterial hypertension is widely discussed. Indeed, the

Genetic determination of arterial hypertension in diabetes mellitus is complex and multifactorial, but given the key role in the pathogenesis of arterial hypertension, renin-aldosterone system and endothelial dysfunction, the genes responsible for the synthesis of

Endothelial dysfunction can manifest itself not only by a disorder of its vascular-motor function, but also by disturbances in the hemostatic system. Markers of endothelial dysfunction can be considered an increase in vilbrand factor and thrombomodulin. When

Chymotrypsin-like proteinases in human blood plasma are normally absent and can enter it from granulocytes or damaged tissues, for example, with hereditary hypercholesterolemia, nonspecific aortoarteritis. Stress induces changes associated with an increase in the content of

Angiotensin II is one of the most powerful vasoconstrictors, which determines its role in the pathogenesis of arterial hypertension. Through the receptor AT II type 1 mediated induction of cell growth. The effect of angiotensin

The presence of contradictory data in the study of genetic determination of arterial hypertension in diabetes mellitus can be explained by differences in the selection criteria and the formation of comparison groups, which to varying