The blood pressure homeostasis in humans is the result of the coordinated interaction of several physiological systems that are affected by many genetic and environmental factors. In many people, these factors combine to produce an elevation in blood pressure or hypertension. Our interest in the regulatory mechanisms determining blood pressure due to the fact that hypertension is a major health problem for people worldwide, causing devastating consequences such as stroke, heart failure and kidney failure.
At present, high blood pressure is detected on a test, which means that can not be diagnosed until it has developed. Recommendations for primary prevention of essential hypertension is currently focused on prevention of the factors that predispose to hypertension, such as obesity, physical inactivity, alcoholism and a high salt intake. Despite these recommendations, if widely accepted by the general public, would result in a healthier population, which are difficult to meet, without the consent of the patient.
Identification of genetic marlers for a predisposition to hypertension in the future may allow intervention focuses on the factors hypertensinogenic. For example, if a person happens to have a genetic predisposition to altered sodium homeostasis introduction in early salt restriction may help prevent hypertension, or at least delay the onset. You can also predict the blood pressure response to specific interventions in lifestyle.
The reactivity of drugs
Effects of drugs are likely to be determined polygenocally. It may be possible to develop genetic markers for individual drug response in the future. This new field called “pharmacogenomics” and may help physicians prescribe individualized treatment empirically to patients with hypertension. There have been several attempts raltae genetic polymorphisms of the therapeutic response. There were also attempts ralate sytem renin gene polymorphisms on the effects of ACE inhibitors in heart, and some genetic variants of diuretic response.
Although much progress has been made in the treatment of hypertension, target organ damage remains a major cause of morbidity and markerdly susceptibility genes may increase the risk of specific complications of hypertension.
In contrast to the many determinants of blood pressure level, it seems likely that the failure of a target organ is the “weak link” in a process of degradation and repair, therefore, fewer genes may predispose an individual complications of hypertension. The genetic determinants for hypertensive organ damage may be closer to our traditional model of inborn errors of metabolism that the complex characteristics of hypertension. Identification of markers allow us to respond quickly to changes irreversible.
Essential hypertension has a complex pathogenesis in which many genetic and environmental factors interact. The identification of genes responsible for monogenic hypertension and physiological dysfunction is still at an early stage. In the future, high throughput techniques will accelerate the pace of discovery. Clinical practice in the treatment of hypertension will be amended by a new understanding of the condition.