Steady-state pharmacokinetics of diltiazem and hydrochlorothiazide administered alone and in combination

Weir, Scott J.; Dimmitt, Dan C.; Lanman, Robert C.; Morrill, M. Bruce; Geising, Dennis H.

doi:10.1002/(sici)1099-081x(199809)19:6<365::aid-bdd112>3.0.co;2-r

Cited by 12 publications

(1 citation statement)

References 14 publications

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“…34 The half-life of HCTZ is 8 to 15 hours with long-term dosing. 33,[35][36][37] The half-life of HCTZ would suggest that the drug should be given twice daily. Several studies, however, support once-daily dosing of HCTZ, demonstrating that the pharmacodynamic response is much longer than predicted by the half-life.…”

Section: Hydrochlorothiazidementioning

confidence: 99%

Hydrochlorothiazide Versus Chlorthalidone

2004

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Abstract-Thiazide diuretics are one of the preferred pharmacologic treatments for hypertension. Hydrochlorothiazide and chlorthalidone have been the 2 most commonly used diuretics in major clinical trials. Treatment guidelines and compendia often consider these 2 drugs interchangeable agents within the class of thiazide or thiazide-like diuretics. Many sources list them as equipotent. Despite these beliefs, there is some suggestion that cardiovascular outcomes are not necessarily the same with these 2 drugs. We conducted a literature search from 1960 to 2003 to identify studies that evaluated the pharmacokinetic and blood pressure-lowering effects of these 2 agents. There are significant pharmacokinetic and pharmacodynamic differences between these diuretics. Chlorthalidone is Ϸ1.5 to 2.0 times as potent as hydrochlorothiazide, and the former has a much longer duration of action. Whether these pharmacokinetic and pharmacodynamic features cause differences in outcomes is not known.

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Section: Hydrochlorothiazidementioning

confidence: 99%

Hydrochlorothiazide Versus Chlorthalidone

2004

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Clinical Relevance of Hepatic and Renal P‐gp/BCRP Inhibition of Drugs: An International Transporter Consortium Perspective

Taskar

Yang

Patel

et al. 2022

Clin Pharma and Therapeutics

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The role of P-glycoprotein (P-gp) and breast cancer resistance protein (BCRP) in drug-drug interactions (DDIs) and limiting drug absorption as well as restricting the brain penetration of drugs with certain physicochemical properties is well known. P-gp/BCRP inhibition by drugs in the gut has been reported to increase the systemic exposure to substrate drugs. A previous International Transporter Consortium (ITC) perspective discussed the feasibility of P-gp/BCRP inhibition at the blood-brain barrier and its implications. This ITC perspective elaborates and discusses specifically the hepatic and renal P-gp/BCRP (referred as systemic) inhibition of drugs and whether there is any consequence for substrate drug disposition. This perspective summarizes the clinical evidence-based recommendations regarding systemic P-gp and BCRP inhibition of drugs with a focus on biliary and active renal excretion pathways. Approaches to assess the clinical relevance of systemic P-gp and BCRP inhibition in the liver and kidneys included (i) curation of DDIs involving intravenously administered substrates or inhibitors; (ii) in vitro-to-in vivo extrapolation of P-gp-mediated DDIs at the systemic level; and (iii) curation of drugs with information available about the contribution of biliary excretion and related DDIs. Based on the totality of evidence reported to date, this perspective supports limited clinical DDI risk upon P-gp or BCRP inhibition in the liver or kidneys.

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