Abstract
Objectives Cilnidipine, an L-/N-type calcium channel blocker (CCB), has unique organ-protective properties due to suppression of hyperactivity in the sympathetic nervous system and renin-angiotensin system (RAS). In this study, we hypothesized that cilnidipine might exert a renoprotective effect by suppressing the RAS. Methods A total of 25 hypertensive patients receiving a RAS inhibitor were randomly assigned to a cilnidipine (n = 12) or amlodipine (n = 13) group. The effects of cilnidipine on proteinuria and angiotensin II–renin feedback were assessed. Results After 6 months of treatment, both systolic and diastolic blood pressures were significantly reduced to a similar extent in both groups. The urine albumin-to-creatinine ratio was significantly lower in the cilnidipine group (p < 0.05) than in the amlodipine group. Amlodipine increased plasma angiotensin I and angiotensin II levels (p < 0.05), whereas cilnidipine did not. Interestingly, the cilnidipine group had a higher ratio of angiotensin-(1–7) (Ang-(1–7)) to angiotensin II in plasma than the amlodipine group (p < 0.05). Conclusions The L-/N-type CCB cilnidipine, but not amlodipine, decreased urinary albumin excretion in hypertensive patients. Cilnidipine also increased the ratio of Ang-(1–7) to angiotensin II in plasma, which might be one factor underlying its beneficial effects.
Highlights
Patients with chronic kidney disease have been shown to have a higher risk of developing cardiovascular diseases and end-stage renal failure as their blood pressure increases [1].erefore, it is crucial to adequately control their blood pressure, initially either with angiotensin-converting enzyme inhibitors or angiotensin II (Ang II) type 1 receptor blockers (ARBs)
Erefore, it is crucial to adequately control their blood pressure, initially either with angiotensin-converting enzyme inhibitors or angiotensin II (Ang II) type 1 receptor blockers (ARBs). In clinical practice, these drugs are often used in combination with a calcium channel blocker (CCB) to achieve a sufficient antihypertensive effect. ere are several types of CCBs that differ according to their duration of action and the calcium channel subtype that they inhibit. e major CCBs exert a strong antihypertensive effect through vasodilation mediated by L-type Ca inhibition, but they can cause reflex stimulation of the sympathetic nervous system and renin-angiotensin system (RAS) by their abrupt hypotensive action
Baseline Characteristics. e baseline characteristics of the subjects are shown in Table 1. ere were no significant differences between the two groups in terms of age, sex, systolic and diastolic blood pressure (BP), heart rate, HbA1c, or total cholesterol level. ere was no additional use of diuretics in either group during the study period
Summary
Patients with chronic kidney disease have been shown to have a higher risk of developing cardiovascular diseases and end-stage renal failure as their blood pressure increases [1].erefore, it is crucial to adequately control their blood pressure, initially either with angiotensin-converting enzyme inhibitors or angiotensin II (Ang II) type 1 receptor blockers (ARBs). E major CCBs exert a strong antihypertensive effect through vasodilation mediated by L-type Ca inhibition, but they can cause reflex stimulation of the sympathetic nervous system and renin-angiotensin system (RAS) by their abrupt hypotensive action. Previous studies showed that cilnidipine demonstrates unique organ-protective properties as a result of its effects on the sympathetic nervous system [4,5,6]. Some previous studies reported that cilnidipine has no effect on plasma renin activity or plasma Ang II levels, while amlodipine, an L-type CCB, significantly increases both parameters [8, 9]. Another study showed that cilnidipine but not amlodipine, suppressed the ARB-induced increase in plasma renin activity and plasma Ang II levels [10]
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