The effect of amlodipin, a calcium channel blocker, on tendon healing: an experimental study in rat model of Achilles tendon injury.

PURPOSE: Achilles tendon injuries represent a major clinical challenge due to the tendon's poor vascularity and limited regenerative capacity. Amlodipine, a dihydropyridine calcium channel blocker, has demonstrated antioxidant, anti-inflammatory, and vasodilatory effects in various tissues. However, its potential influence on tendon healing remains unexplored. This study aimed to evaluate the histopathological and biomechanical effects of amlodipine on tendon regeneration in a rat model of Achilles tendon rupture.

METHODS

Forty-eight male Wistar albino rats (300-350 g) were randomly allocated into four groups (n = 12 each): C14, A14, C28, and A28. A complete Achilles tenotomy was surgically created and repaired using the Kessler technique. Animals received either physiological saline (control) or amlodipine besylate (5 mg/kg/day, oral gavage) for 14 or 28 days. Tendons were harvested for either biomechanical testing (tensile strength and elongation) or histopathological analysis (fibroblastic activity, neovascularization, inflammation).

RESULTS

Amlodipine significantly enhanced fibroblastic activity and neovascularization at both time points compared to controls. Inflammatory scores decreased markedly from day 14 to 28 in the treatment group, indicating a strong anti-inflammatory effect (p < 0.01 for all). Biomechanical testing revealed significantly increased tensile strength (22.23 ± 2.89 N vs. 15.07 ± 3.79 N; p < 0.05) and elongation (4.90 ± 1.62 mm vs. 2.70 ± 0.68 mm; p < 0.05) in the amlodipine group by day 28.

CONCLUSION

Amlodipine appears to accelerate and enhance Achilles tendon healing by promoting fibroblastic proliferation, angiogenesis, and biomechanical strength, while reducing inflammation. These findings suggest a potential role for amlodipine as a pharmacologic adjunct in tendon repair; however, further mechanistic and clinical studies are warranted.