The authors examined the effect of cilnidipine, a unique L/N‐type calcium channel blocker, on abnormal nocturnal blood pressure (BP) dipping in Japanese hypertensive patients in the real world. The Ambulatory Blood Pressure Control and Home Blood Pressure (Morning and Evening) Lowering by N‐Channel Blocker Cilnidipine (ACHIEVE‐ONE), a large‐scale clinical study, was designed to evaluate the effects of cilnidipine in daily medical practice. Among the study, 24‐hour ambulatory BP data were obtained from 615 patients and classified according to their nocturnal dipping status as extreme dippers, dippers, nondippers, or risers. A 12‐week treatment with cilnidipine significantly reduced 24‐hour BP in all groups (P<.001). Changes in nocturnal systolic BP (SBP) from baseline were −17.9 mm Hg from 154.6 mm Hg in risers and −11.9 mm Hg from 142.1 mm Hg, −6.6 mm Hg from 128.5 mm Hg, and 0.1 mm Hg from 115.8 mm Hg in nondippers, dippers, and extreme dippers, respectively. Changes from baseline in nocturnal SBP reduction rate were 8.2% in risers (P<.001) but −7.0% in extreme dippers (P<.001), while no change was observed in the nighttime SBP reduction rate for the total patients (−0.2%±9.6%, P=.617). Cilnidipine partially, but significantly, restored abnormal nocturnal dipping status toward a normal dipping pattern in hypertensive patients.
1. In order to confirm and investigate the hypotensive effect of a high potassium intake we compared mean arterial pressure (MAP), water and electrolyte balance, plasma and urinary noradrenaline (NA), plasma renin activity (PRA) and plasma aldosterone concentration (PAC) in 20 inpatients with mild or moderate essential hypertension on a control diet (Na: 260, K: 75 mmol/day), and after high (K: 175 mmol/day) and low potassium diets (K: 25 mmol/day).
2. After potassium loading, urinary volume (UV) and urinary excretion of sodium (UNaV) and of potassium (UKV) were elevated, and MAP, body weight, plasma volume (PV), extracellular fluid volume (ECFV) and total exchangeable sodium (Nae) were reduced significantly.
3. After potassium loading, PRA, PAC, plasma and urinary NA increased and the pressor response to infused noradrenaline and angiotensin II decreased significantly.
4. The reduction of MAP after potassium loading correlated positively with PV and ECFV during the control period. In addition, significant correlations were found between ΔUV and ΔUNaV, —ΔPV and ΔU/NaV, —ΔPV and Δ plasma NA, and Δ plasma NA and Δ PRA.
5. Patients with low PRA had high PV, ECFV and Nae during the control period, and showed greater reductions of MAP, PV, ECFV and Nae after potassium loading.
6. After potassium restriction, UNaV, PRA and urinary NA decreased and PV increased, and MAP did not change significantly.
7. These results suggest that the hypotensive effect of high potassium intake may be caused by reduction of body fluid volume via augmentation of Na excretion.
In eight patients undergoing chronic hemodialysis, ultrafiltration was performed for 1 h in each patient. The concentration of urea nitrogen, creatinine, ADH, cortisol, GH, prolactin and TSH was measured in plasma and the filtering solution, and the permeability of each substance was determined. The plasma concentration of ADH coincided with that of the filtering solution, and no significant difference was noted between the permeability of creating and ADH. In contrast, cortisol, GH, prolactin and TSH were not detected in the filtering solution. Chromatographic study showed that ADH in the filtering solution coincided with synthetic ADH. From a comparison of the permeability with the molecular weight, it was suggested that ADH in the blood exists in free form without binding with plasma proteins or neurophysin.
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