Systemic hypertension is a major risk factor of ischemic heart disease. However, it can also stimulate mechanisms that protect the heart against acute oxygen deprivation. We study the effects of various forms of hypertension on cardiac ischemic tolerance.
Systemic hypertension is a chronic disease in which the blood pressure in systemic arteries is elevated. Hypertension is one of the major risk factor for ischemic heart disease and its acute form, conventionally known as myocardial infarction. It is well known from clinical studies that about 90% of patients with high blood pressure are categorized as primary hypertension. In this case, high blood pressure is of multifactorial origin and it is not possible to provide any easy explanation of this disease.
The rapid progress in molecular biology and genetics enabled to create many experimental animal models, which are suitable for analysis of individual factors participating in the development of systemic hypertension. However, their effects on myocardial functions and cardiac ischemic tolerance are not yet clearly defined. Recently, the role of these factors was revealed partially, suggesting that not only impaired cardiac ischemic tolerance but also activation of cardioprotective mechanism may occur in hypertensive hearts.
We study the effect of systemic hypertension on cardiac ischemic tolerance in cooperation with researchers from other departments of the Institute of Physiology CAS (Experimental Hypertension, Genetics of Model Diseases), the Faculty of Science Charles University in Prague, Institute of Experimental and Clinical Medicine in Prague and Medical College of Wisconsin in Milwaukee (USA).
Our ongoing projects involve genetic models of systemic hypertension and hypertension models of renal origin. The aims of these projects are to clarify the role of following factors in cardiac ischemic tolerance:
The aim of this project is to investigate if chronic hypoxia increases cardiac ischemic tolerance in rats with systemic hypertension, and if the different or same molecular mechanisms identified earlier in normotensive individuals are involved.