Benidipine, an anti-hypertensive drug, inhibits reactive oxygen species production in polymorphonuclear leukocytes and oxidative stress in salt-loaded stroke-prone spontaneously hypertensive rats

Benidipine reduces ischemia reperfusion-induced systemic oxidative stress through suppression of aldosterone production in mice

“…25 8-OHdG is a sensitive and integral marker of oxidative damage to DNA. Cordis et al 26 reported that 8-OHdG is formed at the onset of reperfusion in the myocardium.…”

Inflammation and Therapy for Hypertension

“…In patients with diabetes and hypertension, it reduces markers of renal inflammation and oxidative stress [44]. Benidipine diminishes oxidative stress and inflammatory cytokines in rat kidney and is cardioprotective in rat autoimmune myocarditis by decreasing inflammation and enhancing NO availability [45]. It is more effective than other DHPs in decreasing NADPH oxidase of primed human mononuclear cells and circulating markers of oxidative stress in patients with essential hypertension [45].…”

“…Benidipine diminishes oxidative stress and inflammatory cytokines in rat kidney and is cardioprotective in rat autoimmune myocarditis by decreasing inflammation and enhancing NO availability [45]. It is more effective than other DHPs in decreasing NADPH oxidase of primed human mononuclear cells and circulating markers of oxidative stress in patients with essential hypertension [45]. Efonidipine may be a potent inhibitor of NF-κB activation in human mesangial cells owing to its dual (L-type and T-type) calcium channel blockade, because the activation of NF-κB by intracellular calcium is independent of L-channel activity.…”

Edaravone, a potent free radical scavenger and a calcium channel blocker attenuate isoproterenol induced myocardial infarction by suppressing oxidative stress, apoptotic signaling and ultrastructural damage

“…Benidipine has been reported to increase the coronary blood flow and suppress Ca+ 2 overloads [Higo et al 1992;Kitakaze et al 1999]. It has also been reported to reduce myocardial necrosis associated with reperfusion after coronary artery ligation [Matsubara et al 2008;Liu et al 2004].…”