Journal of Hypertension: Open Access

Due to its increased risk of heart failure, myocardial infarction, and stroke, hypertension is a significant risk factor for premature death. Antihypertensive medications can lower cardiovascular (CV) morbidity and death. To achieve blood pressure (BP) goals, the majority of hypertensive individuals require more than one antihypertensive medication. Only 20% to 40% of people respond well to monotherapy when trying to lower their blood pressure. The pathophysiology of hypertension is mediated by a number of factors, such as elevated peripheral vascular resistance, elevated cardiac effort, and hypervolemia. Multiple mechanisms can be targeted for increased BP reduction. Because the underlying mechanism causing the BP increase is either different or was previously treated with the lower dose, increasing the dose of a single medication frequently does not have the desired BP-lowering effect. In addition, medications that target various pathways may work to reduce blood pressure. The renin-angiotensinaldosterone system is known to be enhanced by the effects of diuretics and to become active as a response to the decreased circulating blood volume. The renin-angiotensin-aldosterone system is elevated, therefore by combining a diuretic with a renin-angiotensin aldosterone system blocker; blood pressure may be reduced more successfully. If possible side effects of a drug's are vary on dosage, maximum dose may also be effective to reduced B P. Renin-angiotensin-aldosterone system blockers can be added to calcium channel blockers (CCBs) by vein dilation to decrease the occurrence of peripheral oedema that is associated with higher dosages of CCBs. This combination is a potential therapy for the management of hypertension due to the efficiency of enalapril and lercanidipine in lowering blood pressure, the safety profile, and the usage of CCBs and ACE inhibitors together in clinical studies with excellent CV hard end point outcomes.

With increased efforts to improve BP control rates and the emergence of device-based therapies for hypertension, resistive hypertension; defined as blood pressure (BP) remaining above goal despite the use of three or more antihypertensive medications at maximally tolerated doses (one of which should ideally be a diuretic) has received more attention. Patients with true resistant hypertension, controlled resistant hypertension, and pseudo-resistant hypertension make up this classically defined resistant group. The term "apparent" resistant hypertension has been used to identify "apparent" lack of control on 3 medications in studies where pseudo-resistant hypertension cannot be excluded (for example, 24-hour ambulatory BP was not obtained).The prevalence of resistant hypertension has recently been reported in large, well-designed studies. The prevalence of resistant hypertension is 14.8% of treated hypertensive patients and 12.5% of all hypertensives, based on prevalence data from these studies and others in North America and Europe with a combined sample size of more than 600,000 hypertensive participants. However, in terms of identifying risk and estimating benefit from newer therapies like renal denervation, the prevalence of true resistant hypertension; defined as uncontrolled by office and 24-hour ambulatory BP monitoring with confirmed medication adherence; may be more significant. In patients with resistant hypertension, rates of cardiovascular events and mortality follow mean 24-hour ambulatory BPs, with true resistant hypertension representing the highest risk. In large trials, the prevalence of true resistant hypertension has not been directly measured; however, the combined results of a number of smaller studies suggest that true resistant hypertension is present in half of the office-controlled resistant hypertensive patients. Uncontrolled resistant hypertension is prevalent in 10.1% of treated hypertensive patients and 7.9% of all hypertensive patients, according to our pooled analysis.

We aimed to investigate alterations at plasma norepinephrine (NE) levels during rest and exercise and to evaluate tissue Doppler imaging (TDI) parameters in patients with essential hypertension after 6 months from treatment with olmesartan 20 mg. Fourty patients were included in the study. Rest and exercise plasma NE levels were evaluated before and after olmesartan 20 mg treatment. Plasma NE levels were studied by HPLC (high performance liquid chromatography) device. Nevertheless, we examined whether there was a relationship between TDI parameters and plasma NE levels. After 6 months from treatment with olmesartan, rest plasma NE levels (p<0.05) and exercise plasma NE levels (p<0.001) were significantly decreased. Left ventricular mass index (LVMI) and septal myocardial performance index (MPI) were significantly decreased. Systolic septal myocardial velocity (Sm) and early diastolic septal myocardial velocity (Em) were significantly increased. In addition, E/Em ratio, and isovolumetric relaxation time (IVRT) were significantly decreased. Plasma NE levels were seen increased as synchronous with increasing of LVMI. In addition, we observed that plasma NE levels are in relation with LVMI, Sm, Em and E/Em ratio. Consequently, olmesartan treatment, reduces the levels of plasma NE. It also effects on stress-induced systolic and diastolic myocardial functions. These findings support the argument that improvement in myocardial dynamics in patients with HT is related to circulating cathecolamins under stress after angiotensin II receptor subtype 1 blocker therapy.