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. Glomerular hemodynamics were assessed using pressure-natriuresis curves, which were constructed by plotting the urinary excretion of
sodium as a function of the mean arterial pressure, which was calculated as the mean of 48 values based on 24-h monitoring, during the intake of low (3 g NaCl daily) and relatively high (10 g NaCl daily)
sodium diets. Under the relatively high
sodium diet condition,
benidipine significantly lowered systolic and diastolic blood pressure. The pressure-natriuresis curve was steeper after the administration of
benidipine.
Benidipine lowered glomerular capillary hydraulic pressure (P(GC)) levels (from 54.4+/-7.5 to 47.0+/-7.0 mmHg, p=0.0152) and reduced both the resistance of the afferent arterioles (from 10,338+/-2,618 to 9,026+/-2,627 dyn.s/cm5, p=0.047) and the resistance of the efferent arterioles (from 4,649+/-2,039 to 2,419+/-2,081 dyn.s/cm(5), p=0.003). The urinary
albumin excretion rate also decreased after the administration of
benidipine. These findings indicated that
benidipine may be effective for reducing the risk of developing
chronic kidney disease in patients with
metabolic syndrome.