The dihydropyridine ring of the nimodipine is dehydrogenated in the hepatic cells of the liver, a process governed by cytochrome P450 isoform 3A (CYP3A). This can be completely inhibited however, by troleandomycin (an antibiotic) or ketoconazole (an antifungal drug). Excretion
Studies in non-human mammals using radioactive labeling have found that 40–50% of the dose is excreted via urine. The residue level in the body was never more than 1.5% in monkeys. Mode of action
Nimodipine binds specifically to L-type voltage-gated calcium channels. There are numerous theories about its mechanism in preventing vasospasm, but none are conclusive.Nimodipine has additionally been found to act as an antagonist of the mineralocorticoid receptor, or as an antimineralocorticoid. Synthesis
The key acetoacetate (2) for the synthesis of nimodipine (5) is obtained by alkylation of sodium acetoacetate  with 2-methoxyethyl chloride, Aldol condensation of meta-nitrobenzene (1) and the subsequent reaction of the intermediate with enamine (4) gives nimodipine. Stereochemistry
Nimodipine contains a stereocenter and can exist as either of two enantiomers. The pharmaceutical drug is a racemate, an equal mixture of the (R)- and (S)- forms. References
Further reading
Pharmacology: R. Towart, S. Kazda, Br. J. Pharmacol. 67, 409P (1979). Use as cerebral vasodilator: H. Meyer et al., GB 2018134 ; eidem, U.S. Patent 4,406,906 (1979, 1983 to Bayer). Effect on associative learning in aging rabbits: R. A. Deyo et al., Science 243, 809 (1989). External links
"Nimodipine". Drug Information Portal. U.S. National Library of Medicine.
Several hypotheses are given, such as it arises from sinusoidal epithelial damage, increased sinusoidal pressure due to obstruction in blood outflow from the liver, or hepatocellular necrosis.Two morphologic patterns of hepatic peliosis were described by Yanoff and Rawson. In the phlebectatic type, the blood-filled spaces are lined with endothelium and are associated with aneurysmal dilatation of the central vein; in the parenchymal type, the spaces have no endothelial lining and they usually are associated with haemorrhagic parenchymal necrosis. Some consider both patterns to be one process, initiated by focal necrosis of liver parenchyma, observed in parenchymal type, progressing into formation of fibrous wall and endothelial lining around haemorrhage of phlebectatic type. Fibrosis, cirrhosis, regenerative nodules, and tumours may also be seen. Diagnosis
The condition is typically asymptomatic and is discovered following evaluation of abnormal liver function test. However, when severe, it can manifest as jaundice, hepatomegaly, liver failure, and haemoperitoneum. Other cystic conditions of liver
Polycystic liver disease
Solitary congenital cysts
Congenital hepatic fibrosis
Hydatid cyst
Von Meyenburg complexes
Caroli disease (type V choledochal cyst)
Type IV choledochal cysts

Treatment
Treatment is usually directed towards management of the underlying cause. Withdrawal of azathioprine leads to remission in kidney transplant; bacillary peliosis responds to antibiotics. In rare circumstances partial resection of liver or transplant may be required. References


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