# L-type calcium channel blockers at therapeutic concentrations are not linked to CRAC channels and heart failure

**Authors:** Gary S. Bird, Yu-Ping Lin, Charles J. Tucker, Geoffrey Mueller, Min Shi, Sandosh Padmanabhan, Anant B. Parekh

PMC · DOI: 10.1080/10641963.2025.2515924 · Clinical and Experimental Hypertension · 2025-07-12

## TL;DR

This study confirms that amlodipine, a common blood pressure medication, does not activate CRAC channels at therapeutic doses, supporting its continued use.

## Contribution

The study provides evidence that amlodipine does not increase heart failure risk via CRAC channel activation at therapeutic concentrations.

## Key findings

- Amlodipine does not activate CRAC channels at concentrations used in therapy.
- Findings support the safety of amlodipine in hypertension treatment.
- Results align with a previous meta-analysis on amlodipine's safety profile.

## Abstract

Amlodipine has been used as a front-line anti-hypertensive therapy for decades by virtue of blocking voltage-operated calcium channels with high affinity and specificity. Recently, the safety of amlodipine has been questioned, as it was reported to activate Ca2+ release-activated Ca2+ (CRAC) channels and increase the risk of heart failure. Here we show, using a variety of approaches, that amlodipine does not activate CRAC channels at therapeutic concentrations. Combined with our previous meta-analysis, our study should reassure physicians that amlodipine should continue to be prescribed for treating hypertension.

## Linked entities

- **Chemicals:** Amlodipine (PubChem CID 2162)
- **Diseases:** heart failure (MONDO:0005252)

## Full-text entities

- **Diseases:** hypertension (MESH:D006973), heart failure (MESH:D006333)
- **Chemicals:** Amlodipine (MESH:D017311), L-type calcium channel blockers (-)

## Full text

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## Figures

13 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12312753/full.md

## References

50 references — full list in the complete paper: https://tomesphere.com/paper/PMC12312753/full.md

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Source: https://tomesphere.com/paper/PMC12312753