Background: Calcium channel blockers are commonly used to treat hypertension, and are known to generally act on the L-type calcium channel. Recent studies have shown, however, that some calcium channel blockers also block other calcium channel subtypes, including N- and T-type channels. Cilnidipine (CAS 132203-70-4) is an L- and N-type calcium channel blocker, and benidipine hydrochloride (benidipine, CAS 91599-74-5) is known to inhibit the T-type as well as L- and N-type calcium channels. In this study, effects of switching from cilnidipine to benidipine on blood pressure (BP) lowering and renal functions were investigated in order to clarify the physiological properties of the T-type calcium channel.
Methods And Results: Forty hypertensive patients with diabetes and poor BP control despite receiving cilnidipine were selected, and the changes in BP and urine protein (UP) scores were investigated retrospectively after switching from cilnidipine to benidipine for more than 3 months. BP (systolic/diastolic) significantly decreased from 155.8 +/- 13.7 mmHg/76.5 +/- 13.3 mmHg to 145.9 +/- 17.0 mmHg/71.4 +/- 13.7 mmHg after benidipine treatment, and this effect was stably maintained for one year. UP also significantly decreased from 1.29 to 0.67 in the mean score. The decrease in UP may be explained by a mechanism other than BP lowering effect.
Conclusion: These results demonstrate that benidipine has a more potent antihypertensive effect than cilnidipine and also a renoprotective effect, indicating the high usefulness of benidipine in hypertensive patients with diabetes. T-type calcium channel blockade was suggested to be possibly involved in the enoprotective effect of benidipine.
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http://dx.doi.org/10.1055/s-0031-1296643 | DOI Listing |
ACS Appl Mater Interfaces
January 2025
School of Food Science and Engineering, South China University of Technology, Guangzhou 510641, China.
The involvement of neurons in the peripheral nervous system is crucial for bone regeneration. Mimicking extracellular matrix cues provides a more direct and effective strategy to regulate neuronal activity and enhance bone regeneration. However, the simultaneous coupling of the intrinsic mechanical-electrical microenvironment of implants to regulate innervated bone regeneration has been largely neglected.
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