The homeostasis of human blood pressure results from coordinated interactions of several physiological systems influenced by many genetic and environmental factors.
In many people, these factors together contribute to an increase in blood pressure or high blood pressure. Our interest in determining the mechanisms of blood pressure regulation is based on the fact that high blood pressure is a major public health problem worldwide and has devastating consequences such as stroke, heart failure, and kidney failure.
Currently, high blood pressure is detected by screening, which means it can not be diagnosed until it has developed. The recommendations for the primary prevention of essential hypertension are currently aimed at avoiding predisposing factors for hypertension, such as obesity, physical inactivity, alcoholism, and excessive salt intake. Although such recommendations, if accepted by the general public, would lead to a healthier population, they are difficult to meet without patient compliance.
Future identification of genetic vectors for susceptibility to high blood pressure may allow the targeted intervention of these hypertensive factors. For example, if it is determined that an individual has a genetic predisposition to impaired sodium homeostasis, early introduction of the salt restriction may help prevent hypertension or at least delay the onset of hypertension. of the disease. We can also predict the response of blood pressure to certain lifestyle measures.
Reactivity to drugs
The effects of the drug are probably polygonal. It may be possible in the future to develop gene markers for the individual response to drugs. This new area, called “pharmacogenomics”, will likely help clinicians prescribe more individualized empiric therapy for hypertensive patients. Several attempts have been made to relate genetic polymorphisms to drug response. It has also been attempted to correlate the polymorphisms of the renin-angiotensin system genes with effects on ACE inhibitors of the heart and some variants of the gene with the response to diuretics.
target organ protection
Although much progress has been made in the treatment of hypertension. Target organ damage remains a major cause of morbidity. Susceptibility genes may significantly increase the risk of certain hypertensive complications.
Unlike many determinants of blood pressure. It seems likely that target organ failure is the “weakest link” in a process of injury and repair. As a result, fewer genes could predispose an individual to hypertensive complications. The genetic determinants of hypertensive organic lesions may be closer to our traditional pattern of congenital metabolic disorders than to the complex feature of hypertension. By identifying the markers, we may be able to intervene early before irreversible changes occur.
Essential hypertension has complex pathogenesis, in which many genetic and environmental factors interact. The identification of the genes responsible for monogenic hypertension. Their physiological dysfunction is still in its infancy. In the future, broadband techniques will accelerate the pace of discovery. Clinical practice in the treatment of high blood pressure is being modified by a new understanding of the disease.