In the present study, we investigated the change in renal hemodynamics induced by a calcium antagonist in young (6 weekold) spontaneously hypertensive rats (SHR), a saltsensitive hypertensive model. In acute experiments, SHR were fed either a 0.66% or 8.0% NaCl diet for 4 weeks. In acute experiments, manidipine, a calcium antagonist, was administered in a bolus dose of 10μg/kg. In chronic experiments, SHR were fed a 0.66% NaCl, 0.66% NaCl plus 0.05% manidipine, 8.0% NaCl or 8.0% NaCl plus 0.05% manidipine diet for 4 weeks. Mean arterial pressure (MAP), glomerular filtration rate (GFR), and renal blood flow (RBF) were measured. Salt loading increased MAP in young SHR. Acute administration of manidipine decreased MAP more in saltloaded SHR compared to nonsaltloaded SHR (-43.3±3.1 vs. -18.6±2.1mm Hg: p<0.01). Moreover, chronic administration of manidipine attenuated the rise in MAP in saltloaded SHR (155±3mm Hg vs. 196±5mm Hg: p<0.01) and less so in nonsaltloaded SHR (150±2mm Hg vs. 160±3mm Hg: p<0.01). Salt loading elevated renal vascular resistance (RVR) but changed neither RBF nor GFR. The acuteand chronicadministration of manidipine increased RBF (Acute; +0.77±0.22m
l/min/g kidney: p<0.05, Chronic; 4.32±0.29 vs. 5.50±0.90m
l/min/g kidney: p<0.01) in nonsaltloaded SHR, which was greater in saltloaded SHR (Acute; +2.19±0.52ml/min/g kidney: p<0.05 vs. nonsaltloaded SHR, Chronic; 4.29±0.53 vs. 6.09±1.41m
l/min/g kidney: p<0.01) Manidipine also decreased RVR (Acute; -10.2±2.2mm Hg/m
l/min/g kidney: p<0.01, Chronic; 35.3±1.6 vs. 27.3±4.1mm Hg/ml/min/g kidney: p<0.01) in nonsaltloaded SHR, which was greater in saltloaded SHR (Acute; -21.1±3.1mm Hg/m
l/min/g kidney: p<0.01 vs. nonsaltloaded SHR, Chronic; 44.9±2.6 vs. 27.6±4.1mm Hg/m
l/min/g kidney: p<0.01). GFR did not change significantly following manidipine. It is suggested that the antihypertensive effect of the calcium antagonist, manidipine, was greater in saltloaded SHR and was accompanied by profound amelioration of the abnormal renal hemodynamics.
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