Essential hypertension (EH) is a polygenic and multifactorial disorder that results from genetic and/or environmental factors (Lifton et al., 2001). This disease has no identifiable origin, but results from a disturbance of systems regulating blood pressure (BP) such as several circulating and local neurohumoral and vasoactive factors. Genetic variations of these factors could play a role in the genesis of EH which represents a major risk factor for ischemic heart disease, stroke, peripheral vascular disease and progressive renal damage (Mesrati, 2007). EH rises with age, and it aggregates with other cardiovascular risk factors, such as dyslipidaemia, glucose intolerance, hyperinsulinaemia, abdominal obesity, and hyperuricaemia. Other environmental factors influence this disease like high dietary intake of sodium, alcohol, and stress. Family history, appears to play a major role because EH is more likely to develop in individuals when there is a strong family history. Several studies have identified a variety of candidate genes in EH as well as their interaction with one another and with the environment. Among these hypertension-predisposition genes investigated, genes involved in the renin-angiotensin-aldosterone system, catecholaminergic/adrenergic function, genes of signal transduction system as G protein ┚3subunit, sodium channel system, ┙ adducin and atrial natriuretic peptides. Several other biomarkers have been reported to increase the ability to predict EH such as hormone receptors like glucagon receptor and insulin like growth factor 1 (O’Shaughnessy, 2001, Timberlake et al., 2001) and other systems as endothelin, apolipoprotein and cytokine systems. In this chapter, we expose the genetic markers of EH and their expression related to lifestyle through several strategies such as investigation of specific candidate genes, genome-wide searches, use of intermediate phenotypes, comparative genomics and a combination of these methods (Timberlake et al., 2001)