{'fraction_non_alphanumeric': 0.012711864406779662, 'fraction_numerical': 0.0, 'mean_word_length': 5.946078431372549, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
[The role of insulin resistance in pathogenesis of arterial hypertension].

Arterial hypertension (AH) is a major challenge facing modern medicine. High frequency of AH patients with excess body mass and disturbances ofcarbohydrate metabolism is attributable to their common pathophysiological mechanisms underlain by insulin resistance and resulting compensatory hyperinsulinemia. The authors review modern concepts of AH development in patients with insulin resistance associated with enhanced blood insulin level and increased production of catecholamines playing an important role in AH pathogenesis mediated through sympathetic stimulation of heart, vessels while kidneys. Insulin resistance contributes to AH largely by activating sympathoadrenal system while increased glomerular filtration of glucose is accompanied by its back absorption together with sodium in proximal tubules. It results in hypervolemia and enhanced content of sodium and calcium in vascular walls which leads to their spasm and a rise in the total peripheral vascular tension (TP VT). Insulin promotes fibroblast proliferation and vascular smooth muscle cells via stimulation of tissue growth factors and collagen synthesis in atherosclerotic plaques. The concomitant narrowing of the vessels further increases TPVT. It in turn decreases renal blood flow and thereby activates renin-angiotensin-aldosterone system and development of AH.