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Does smoking influence the pharmacokinetics and pharmacodynamics of the H2‐receptor antagonist famotidine?
Author(s) -
Baak LC,
Ganesh S,
Jansen JB,
Lamers CB
Publication year - 1992
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/j.1365-2125.1992.tb04025.x
Subject(s) - famotidine , pharmacodynamics , pharmacokinetics , medicine , placebo , antagonist , pharmacology , smoking cessation , histamine h2 receptor , crossover study , receptor antagonist , receptor , alternative medicine , pathology
Twelve healthy habitual cigarette smokers and eight non‐smokers participated in a double‐blind placebo controlled study to determine the effect of smoking on the pharmacokinetics and pharmacodynamics of the H2‐receptor antagonist famotidine. In smokers, cigarette smoking was standardised and started 1 h before (A), or 2 h after (B) drug administration, or was prohibited (C). Intragastric pH‐levels (IGpH) were measured with an ambulatory pH‐recorder. Famotidine (40 mg orally) significantly raised median 22 h IGpH in non‐smokers and smokers in all study periods. The smoking sequence (A, B, C) did not significantly influence median 22 h IGpH in both placebo‐treated and famotidine‐ treated smokers, and no significant difference in median 22 h IGpH was shown between smokers and non‐smokers. Plasma drug concentrations were similar in the various experiments, although famotidine was detected earlier in plasma from non‐smokers compared with smokers (P less than 0.05). Smoking did not interfere significantly with the pharmacokinetics and pharmacodynamics of famotidine.