Clinical utility of fixed-dose combinations in hypertension: evidence for the potential of nebivolol/valsartan

Abstract

Despite significant advances in pharmacologic approaches to treat hypertension during the last decades, hypertension- and hypertension-related organ damage are still a high health and economic burden because a large proportion of patients with hypertension do not achieve optimal blood pressure control. There is now general agreement that combination therapy with two or more antihypertensive drugs is required for targeted blood pressure accomplishment and reduction of global cardiovascular risk. The goals of combination therapies are to reduce long-term cardiovascular events by targeting different mechanism underlying hypertension and target organ disease, to block the counterregulatory pathways activated by monotherapies, to improve tolerability and decrease the adverse effects of up-titrated single agents, and to increase persistence and adherence with antihypertensive therapy. Multiple clinical trials provide evidence that fixed-dose combinations in a single pill offer several advantages when compared with loose-dose combinations. This review discusses the advances in hypertension control and associated cardiovascular disease as they relate to the prospect of combination therapy targeting a third-generation beta (β) 1-adrenergic receptor (nebivolol) and an angiotensin II receptor blocker (valsartan) in fixed-dose single-pill formulations.

Combination of β Adrenergic Receptor Block and Renin–Angiotensin System Inhibition Diminished the Angiotensin II-Induced Vasoconstriction and Increased Bradykinin-Induced Vasodilation in Hypertension

“…For example, nebivolol, a third-generation b 1 adrenergic blocker, offers an additional BP reduction when it was administered in a combination therapy or as an add-on drug to the ongoing therapy with ACEI or ARA. 26 There are few studies that describe the use of propranolol in combination with cilazapril or captopril, and results show that both combinations reduced SBP, DBP, and plasmatic renin activity. 27,28 One of the mechanisms that could explain the antihypertensive effect is through changes in the vascular reactivity.…”