Key result
Azelnidipine improves insulin resistance and glucose tolerance in hypertensive patients with metabolic disorders by potentially inhibiting sympathetic nerve activity.
Why the study?
Does azelnidipine improve glucose tolerance and insulin resistance in hypertensive patients with metabolic disorders?
Does azelnidipine improve glucose tolerance and insulin resistance in hypertensive patients with metabolic disorders?
Azelnidipine may offer cardioprotective and anti-atherogenic benefits beyond blood pressure lowering for hypertensive patients with metabolic disorders.
May support azelnidipine consideration in hypertensive patients with metabolic disorders; leaves open confirmation in prospective randomized trials.
Azelnidipine is a unique dihydropyridine calcium channel blocker with selectivity for L-type calcium channels that has been launched for the treatment of hypertension. Azelnidipine exhibits long-acting blood pressure-lowering effects without increasing heart rate. High blood pressure is associated with many metabolic disorders, including glucose intolerance and insulin resistance. Antihypertensive medications that interfere with various steps in the renin-angiotensin system improve glucose tolerance and insulin resistance; however, the effects of calcium channel blockers on glucose metabolism and insulin resistance remain controversial. Recent studies have demonstrated that azelnidipine could improve insulin resistance and glucose tolerance by potentially inhibiting sympathetic nerve activity. In addition, azelnidipine exhibits anti-inflammatory and anti-oxidative effects, suggesting that it is a beneficial antihypertensive agent with anti-atherogenic and cardioprotective effects for the treatment of not only hypertensive patients with glucose intolerance, but also those with metabolic disorders.
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Shimada et al. (2014) conducted a review in Hypertension with metabolic disorders. Azelnidipine was evaluated. Azelnidipine improves insulin resistance and glucose tolerance in hypertensive patients with metabolic disorders by potentially inhibiting sympathetic nerve activity.
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