br Acknowledgements br Introduction Resistant hypertension R

Acknowledgements
Introduction Resistant hypertension (RH), is defined as blood pressure (BP) > 140/90 mm Hg despite three full doses antihypertensive drugs including a diuretic. Controlled hypertensive patients taking four Hordenine or more of antihypertensives are also considered resistant (Calhoun et al., 2008). Those with resistant hypertension have double the risk of cardiovascular events than those without resistant hypertension, thus making them an important group to study (Daugherty et al., 2012). More recently, the studies of Xavier indicates that, On 15 million known hypertensive, 12 are treated with drugs, but the blood pressure is controlled only in half. And a hypertensive on two does not know his state (Girerd, 2011). However, the prevalence of resistant hypertension has been estimated to be 20% to 30% (Calhoun et al., 2008). The interindividual variability observed in response to antihypertensive drugs represents a significant source of failure in treatment (LEFEBVRE, 2008). Although there are many data of studies demonstrating the effectiveness of the antihypertensive drug therapy in the general population. In fact, each hypertensive seems to have its own way of reacting to the drug (Ninomiya et al., 2008). In addition to the pathway of drug absorption, metabolism, and excretion, candidate genes involved in the disease relevant pathways may also influence the clinical response to treatment. The renin–angiotensin system (RAS) is one of the major regulators in BP homeostasis. Inhibiting RAS, with angiotensin I converting enzyme inhibitors (IEC) and angiotensin type-1 receptor blockers (ARAII), has long been known as one of the most successful therapies for the management of hypertension. Some polymorphisms in genes of RAS are associated with BP regulation and influence the BP response to antihypertensive drugs (Sciarrone et al., 2003; Kurland et al., 2001). ACE enzyme involved in conversion the Angiotensin I to Angioensin II after a cascade the reaction, angiotensin II exerts numerous effects on the homeostatic regulation of blood pressure, the vast majority of which are mediated via the angiotensin II type 1 receptor (AT1R) (Gong et al., 2012). The ACE gene is mapped on chromosome 17q23, and is encoded by a 21 Kb gene that consists of 26 exons and 25 introns (Di Pasquale et al., 2005). A polymorphism of the ACE gene has been largely described, and consists of a 287 pb Alu repeat sequence Insertion (I) or Deletion (D), near the 3′ end of intron 16, producing three genotypes (II homozygote, ID heterozygote and DD homozygote) (Rigat et al., 1990). Which the D allele results in a higher gene expression, and seems to be associated with increased risk for hypertension (Stephens et al., 2005; Zarouk et al., 2012). The aim of the present study was to investigate the association of I/D polymorphisms of ACE gene is associated with resistant hypertension and essential controlled hypertension.
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