Benidipine Attenuates Glomerular Hypertension and Reduces Albuminuria in Patients with Metabolic Syndrome

Abstract

Recent studies have shown that metabolic syndrome is associated with an increased risk for chronic kidney disease. We recently found that the prevalence of sodium-sensitive hypertension in patients with metabolic syndrome was significantly higher than that in patients with essential hypertension but without metabolic syndrome. We therefore assessed the effects of benidipine, a long-acting calcium channel blocker, on the sodium sensitivity of blood pressure and renal hemodymamics in 5 patients with metabolic syndrome.

Effects of febuxostat on metabolic and renal alterations in rats with fructose-induced metabolic syndrome

“…In addition, recent studies in humans have shown that metabolic syndrome is associated with an increased risk for a reduced GFR and microalbuminuria (9,20). Interestingly, it has been reported that patients with essential hypertension and metabolic syndrome have glomerular hypertension and increased albumin excretion (52).…”

Effects of combination therapy with angiotensin II type I receptor blockers and calcium channel blockers on renal function in hypertensive patientsA retrospective, “real-world” comparative study

“…Some CCBs,however,selectivelydilaterenalafferentarteriolesr athert hane fferentarterioles,a nd therebyincreasei ntra-glomerularpressure, possiblyleading tothe developmentorfurtherprogression of nephropathy [16].Benidipine hasbeen shownto improvethe vascularr esistanceo frenale fferentarteriolesand toreducei ntra-glomerularpressurei nanimal models [16], hypertensivep atients withn ephropathy [17]a nd thosewithm etabolicsyndrome [18].Amlodipine and nifedipine,in contrast,do notdilaterenale fferentarterioless om arkedlyast heydilateafferentarterioles,a ccording too ne report [16].Furthermore, benidipine hasinhibitory effects on aldosterone production viab lockade of T-type voltage-dependentCa 2+ channels [19]a nd on the urinary protein excretion occurring in responseton itricoxide (NO)p roduction whichi smediated byBH 4 (tetrahydrobiopterin) [20]. Theserenalp rotectivee ffects of benidipine mayaccountfort he differencei nrenale ventr atesobserved among the CCBsin the presentclinicalstudy.Benidipine morem arkedlydecreasesBP and urinary protein thanamlodipine,a ss howni naprevious study [11 -13].…”

Mechanism underlying the block of human Cav3.2 T-type Ca2+ channels by benidipine, a dihydropyridine Ca2+ channel blocker

“…In addition, benidipine causes dilation of renal efferent arterioles and inhibition of aldosterone production, which cannot be explained by the block of L-type Ca 2+ channels. (Kawata et al, 1997;Morikawa et al, 2002;Uzu et al, 2007;Akizuki et al, 2008). These pharmacological effects appear to be due to the additional block of T-type Ca 2+ channels.…”