Nifedipine is completely absorbed after oral administration. Plasma drug concentrations rise at a gradual, controlled rate exhibiting zero-order absorption kinetics after nifedipine administration and reach a plateau at approximately 6 hours after the first dose. For subsequent doses, relatively constant plasma concentrations at this plateau are maintained with minimal fluctuations over the 24-hour dosing interval. About a 4-fold higher fluctuation index (ratio of peak to trough plasma concentration) was observed with the conventional immediate release Adalat capsule at t.i.d. dosing than with once daily Adalat XL tablets. At steady state the bioavailability of the Adalat XL tablet is 86% relative to Adalat capsules. Administration of the Adalat XL tablet in the presence of food slightly alters the early rate of drug absorption, but does not influence the extent of drug bioavailability. Markedly reduced gastrointestinal retention time over prolonged periods (i.e., short bowel syndrome), however, may influence the pharmacokinetic profile of the drug which could potentially result in lower plasma concentrations. Pharmacokinetics of Adalat XL tablets are linear over the dose range of 30 to 180 mg in that plasma drug concentrations are proportional to dose administered. There was no evidence of dose dumping either in the presence or absence of food. The bioavailability of the 20 mg tablet is directly proportional to the 30 mg tablet.

Nifedipine is extensively metabolized to highly water-soluble, inactive metabolites accounting for 60 to 80% of the dose excreted in the urine. The remainder is excreted in the feces in metabolized form, most likely as a result of biliary excretion. The main metabolite (95%) is the hydroxycarbolic acid derivative, the remaining 5% is the corresponding lactone. Only traces (less that 0.1% of the dose) of unchanged nifedipine can be detected in the urine. Thus, the pharmacokinetics of nifedipine are not significantly influenced by the degree of renal impairment. Patients in hemodialysis or CAPD (continuous ambulatory peritoneal dialysis) have not reported significantly altered pharmacokinetics of nifedipine.

Since hepatic biotransformation is the predominant route for the disposition of nifedipine, the pharmacokinetics may be altered in patients with chronic liver disease. Pharmacokinetic studies in patients with hepatic cirrhosis showed a clinically significant prolongation of elimination half-life and a decrease in total clearance of nifedipine. The degree of serum protein binding of nifedipine is high (92 to 98%). Protein binding may be greatly reduced in patients with renal or hepatic impairment .

Nifedipine is metabolized by the cytochrome P450 enzyme system, predominantly via CYP3A4, but also by CYP1A2 and CYP2A6 isoenzymes.

Compounds found in grapefruit juice inhibit the cytochrome P450 system, especially CYP3A4. In a grapefruit juice-nifedipine interaction study in healthy male volunteers, pharmacokinetics of nifedipine showed significant alteration. Following administration of a single dose of nifedipine 10 mg with 250 mL of grapefruit juice, the mean value of nifedipine AUC increased by 34% and the t_max increased from 0.8 to 1.2 hours, as compared to water .