Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.

Karasawa, Akira; Kubo, Kazuhiro

doi:10.1254/jjp.52.553

Cited by 26 publications

(19 citation statements)

References 23 publications

(22 reference statements)

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“…Effective inhibition of DOX or daunorubicin-mediated lipid peroxidation by verapamil or nifedipine was observed in previous studies. 18,19 Furthermore, Karasawa et al 22 have found that benidipine, a new type of dihydropyridine derivative, which has more longlasting effects through its interaction with lipid membranes 43 protects acute ischemic renal failure in rats by inhibiting lipid peroxidation and calcium overload. Therefore, we speculate that inhibition of lipid peroxidation of the membranous system in cardiac myocytes by benidipine may inhibit DOX-induced impairment of the mobilization and removal of intracellular free Ca 2+ ions and the -adrenoceptor responsiveness of Ca 2+ handling.…”

Section: Discussionmentioning

confidence: 99%

“…[15][16][17] Other reports have shown that calcium antagonists effectively inhibit anthracycline-mediated lipid peroxidation. 18,19 Furthermore, recent studies on brain and kidney have reported that antiischemic effects of calcium antagonists may be explained by inhibition of lipid peroxidation [20][21][22] and that the lipophilicity of long-acting calcium antagonists can enhance their antioxidant activity. 20,23 Therefore, the effects of calcium antagonists against DOX-induced cardiotoxicity are not yet well evaluated.…”

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confidence: 99%

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A Calcium Antagonist Protects against Doxorubicin-Induced Impairment of Calcium Handling in Neonatal Rat Cardiac Myocytes

et al. 1999

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

A Calcium Antagonist Protects against Doxorubicin-Induced Impairment of Calcium Handling in Neonatal Rat Cardiac Myocytes

et al. 1999

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“…In rats with acute ischemic renal failure, intravenous treatment with benidipine (10 µg/ kg) suppressed elevation in serum creatinine and blood urea nitrogen, the reduction in renal ATP, the elevation in lipid peroxide, and the elevation in intracellular calcium levels following reperfusion (64). These effects of benidipine were more potent than those of other DHP- derived CCBs such as nifedipine, nitrendipine, and amlodipine (64,65).…”

Section: Renoprotective Effectsmentioning

confidence: 94%

Pharmacological, Pharmacokinetic, and Clinical Properties of Benidipine Hydrochloride, a Novel, Long-Acting Calcium Channel Blocker

Yao

Nagashima

Miki³

2006

J Pharmacol Sci

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Abstract. Benidipine is a dihydropyridine-derived calcium channel blocker developed in Japan, with several unique mechanisms of action, that is, triple calcium channels (L, N, and T) blocking action with a membrane approach. Benidipine has relatively high vascular selectivity and is expected to show protective effects on vascular endothelial cells. Renal protective effects of benidipine also have been shown in several basic and clinical studies. Moreover, anti-oxidative action and enhancing nitric oxide production have been noted with this drug, following its cardioprotective effects in patients with ischemic heart diseases. In fact, benidipine exerted a better prognostic effect than other calcium channel blockers in the therapy for patients with vasospastic angina. In addition, benidipine showed reliable antihypertensive, renoprotective effects if used in combination with angiotensin II type 1 receptor blockers (ARBs) when adequate anti-hypertensive effects are not achieved by ARBs alone, indicating that benidipine is an useful calcium channel blocker in combination therapy for hypertension. Benidipine was launched on the Japanese market 14 years ago, but few severe side effects have been reported, suggesting that this is a drug with established safety and long-acting pharmacological effects.

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“…Histological analysis of tuburointerstitial lesions 94 days after induction of the nephrotic syndrome in vehicle and benidipine (1 or 3 mg/kg, p.o. )-treated rats DISCUSSION Ca-channel blockers, including benidipine, have ameliorating effects on renal function in various animal models of renal failure (2)(3)(4)17). Therefore, Ca-chan nel blockers can be expected to be drugs for protecting against the renal injury.…”

Section: Methodsmentioning

confidence: 99%

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

Shirakura

Sano

Karasawa

et al. 1992

Japanese Journal of Pharmacology

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ABSTRACT-An experimental focal segmental glomerular sclerosis (FSGS) was induced by the com bined administration of puromycin aminonucleoside (PAN) and protamine sulfate (PS). Blood collec tions were made on days 0, 37, 70 and 94. Urine collections were made on days 0, 24, 80 and 94. Vehicle-treated rats showed severe proteinuria and an increase in serum total cholesterol (sTC). Benidi pine (1 or 3 mg/kg, p.o.)-treated rats exhibited less proteinuria and lower sTC than the vehicle-treated rats. On days 70 and 94, both blood urea nitrogen (BUN) and serum creatinine (sCR) values in the vehicle-treated rats were significantly higher than those in normal rats (without treatment with PAN and PS). On the other hand, the treatment with benidipine (1 or 3 mg/kg, p.o.) attenuated the in creases in BUN and sCR. On day 94, vehicle-treated rats showed a significant decrease in creatinine clearance as compared with normal rats, but benidipine (1 or 3 mg/kg, p.o.)-treated rats did not. The histology was examined on day 94. Vehicle-treated rats demonstrated a significantly greater percentage of glomeruli with segmental areas of glomerulosclerosis/hyalinosis, mesangial cell proliferation, and mesangial foam cell. Benidipine (3 mg/kg, p.o.) ameliorated the development of renal regeneration as estimated by histological examination. These results suggest that the Ca-channel blocker benidipine is a favorable drug for preventing the progression of glomerular sclerosis.

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Protection by benidipine hydrochloride (KW-3049), a calcium antagonist, of ischemic kidney in rats via inhibitions of Ca-overload, ATP-decline and lipid peroxidation.

Abstract: Abstract-Renal failure was produced in rats by unilateral clamping of the left renal artery for 60 min, followed by reperfusion and contralateral nephrectomy.

Cited by 26 publications

References 23 publications

A Calcium Antagonist Protects against Doxorubicin-Induced Impairment of Calcium Handling in Neonatal Rat Cardiac Myocytes

A Calcium Antagonist Protects against Doxorubicin-Induced Impairment of Calcium Handling in Neonatal Rat Cardiac Myocytes

Pharmacological, Pharmacokinetic, and Clinical Properties of Benidipine Hydrochloride, a Novel, Long-Acting Calcium Channel Blocker

Protective Effect of Benidipine against the Development of Glomerular Sclerosis in Experimental Nephrotic Syndrome

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