Plendil can affect this through 2 different nutrient pathways: Calcium, Potassium. This medication is commonly used for Hypertension.
Each nutrient below contributes to this impact through a different mechanism.
Low calcium levels overstimulate nerves and muscles, leading to muscle cramps, spasms, and twitching. More significant deficiency can cause tetany, a state of sustained, painful muscle contractions often with carpopedal spasms and tingling around the mouth, hands, and feet. In severe cases, untreated hypocalcemia may progress to breathing difficulties from laryngospasm, seizures, abnormal heart rhythms, and other potentially life‑threatening complications.
Agrawal A, Suryakumar G, Rathor R. Role of defective Ca2+ signaling in skeletal muscle weakness: Pharmacological implications. J Cell Commun Signal. 2018 Dec;12(4):645-659. Uday S, Högler W. Nutritional Rickets and Osteomalacia in the Twenty-first Century: Revised Concepts, Public Health, and Prevention Strategies. Curr Osteoporos Rep. 2017 Aug;15(4):293-302. Basma A. Dahash, et al. Rickets. StatPearls August 7, 2023. Seema M. Policepatil, et al. Hypocalcemic Myopathy Secondary to Hypoparathyroidism.Aloke A, Singh K. An Unusual Presentation of Multifactorial Hypocalcemia as Myopathy: A Case Report. Cureus. 2025 Jul 7;17(7):e87434.
Potassium deficiency can progress from diffuse muscle weakness to flaccid paralysis, and in severe hypokalemia this paralysis may involve the diaphragm and other respiratory muscles, resulting in hypoventilation and acute respiratory failure. In these situations, patients often present with ascending weakness, areflexia, and shortness of breath or an inability to take a deep breath, and may require urgent ventilatory support while intravenous potassium is carefully replaced. Case reports and cohort data show that even admission potassium values just below the normal range are associated with a higher risk of needing mechanical ventilation in hospitalized patients, underscoring the importance of promptly recognizing and correcting hypokalemia before it reaches paralysis‑level severity.
Sobrosa P Sr, Ferreira Â, Vilar da Mota R, Couto J, Sousa L. Severe Hypokalemia and Respiratory Muscle Paralysis: An Atypical Manifestation of Primary Sjögren's Syndrome. Cureus. 2024 Dec 23;16(12):e76240. Alemu GK, Asfaw SA, Asres LS, Kassa BY. Severe Life-Threatening Hypokalemia Primarily Presented With Isolated Paralysis: Case Series From Ethiopia. Clin Case Rep. 2025 Jan 6;13(1):e70062. Pande AR, Rai N, Manchanda S, Srivastava A, Agarwal S, Srivastava IC, Awasthi A. The Critical Care Phenotype of Hypokalemic Paralysis: Etiology, Outcomes, and Predictors of Respiratory Failure in a Retrospective Cohort Study. Cureus. 2026 Feb 18;18(2):e103865. Gombar S, Mathew PJ, Gombar KK, D'Cruz S, Goyal G. Acute respiratory failure due to hypokalaemic muscular paralysis from renal tubular acidosis. Anaesth Intensive Care. 2005 Oct;33(5):656-8.
Some side effects may be linked to nutrient depletion caused by this medication.
Studies suggest that Felodipine, a type of calcium channel blocker (CCB), may increase the excretion of calcium in the urine. While the long-term effects on bone health are unclear, some healthcare professionals suggest calcium supplementation for patients taking felodipine, especially those at higher risk of osteoporosis.
Research suggests that Felodipine, a type of calcium channel blocker (CCB), may increase the excretion of magnesium in the urine. This can potentially lead to magnesium deficiency. Studies have shown an increase in fractional excretion of magnesium following felodipine treatment, and the drug may also alter how magnesium moves across red blood cell membranes. Therefore supplementation with magnesium should be considered when on this therapy.
An increased excretion of potassium can occur in people taking calcium channel blocker drugs like felodipine. Supplementation may need to be considered if blood levels of potassium are low.