Do the metabolic effects of beta blockers make them leading or supporting antihypertensive agents in the treatment of hypertension?

Reduction of blood pressure to guideline goals (i.e., <130/80 mm Hg) in persons with diabetes is crucial to optimally reduce cardiovascular events and kidney disease progression. Since many patients will be >20/10 mm Hg above this goal, most guidelines recommend using agents that block the renin-angiotensin system in concert with a thiazide-like diuretic to achieve goal blood pressure. Meta-analyses of clinical trials indicate that while all classes of antihypertensive agents reduce cardiovascular risk, they exert different effects on glucose utilization and lipids and, hence, may affect morbidity. Specifically, beta blockers, in general, worsen insulin resistance and increase triglycerides in a dose-dependent fashion. Moreover, they are not recommended as initial therapy for hypertension treatment in the absence of heart failure or recent myocardial infarction, especially in the elderly. Recent studies support the notion that newer beta blockers with vasodilating effects have a better metabolic profile when compared with those that purely affect beta receptors. Thus, vasodilating beta blockers, by being neutral on glycemic and metabolic factors, are associated with less use of additional medication for lipid or glucose control and may provide a potentially greater cardiovascular risk reduction by virtue of these effects.