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Angiotensin-converting enzyme pharmacokinetics

Clinical pharmacokinetics of the angiotensin converting enzyme inhibitors, Clin. Pharmacokinet. 1985, 20, 377-399. [Pg.130]

Table 8.1 Pharmacokinetic details of angiotensin-converting enzyme (ACE) inhibitors used for treatment of hypertension... Table 8.1 Pharmacokinetic details of angiotensin-converting enzyme (ACE) inhibitors used for treatment of hypertension...
Ding PY, Hu OY, Pool PE, Liao W. Does Chinese ethnicity affect the pharmacokinetics and pharmacodynamics of angiotensin-converting enzyme inhibitors J. Hum Hypertens 2000 14(3) 163-70. [Pg.235]

Jacolot A, Tod M, Petitjean O. Pharmacokinetic interaction between cefdinir and two angiotensin-converting enzyme inhibitors in rats. Antimicrob Agents Chemother 1996 40(4) 979-82. [Pg.700]

Sica DA, Gehr TW. The pharmacokinetics of angiotensin-converting enzyme inhibitors in end-stage renal disease. Semin Dialysis 1994 7 205-213. [Pg.819]

E Ezan et al. Enzyme immunoassays for a new angiotensin converting enzyme inhibitor, zabicipril, and its active metabolite in human plasma—Application to pharmacokinetic studies. Ther Drug Monit 15 448, 1993. [Pg.319]

Celecoxib is currently indicated for the relief of signs and symptoms of osteoarthritis and rheumatoid arthritis and to reduce the number of adenomatous colorectal polyps in familial adenomatous polyposis as an adjunct to usual care. Celecoxib is at least as effective as naproxen in the symptomatic management of osteoarthritis and at least as effective as naproxen and diclofenac in the symptomatic treatment of rheumatoid arthritis, and it is less likely to cause adverse Gl effects. Celecoxib appears to be effective in the management of pain associated with both of these arthritic conditions, but effectiveness in acute or chronic pain has not been fully demonstrated. Unlike aspirin, celecoxib does not exhibit antiplatelet activity. Concomitant administration of aspirin and celecoxib may increase the incidence of Gl side effects. Another notable potential drug interaction with celecoxib is its ability, like other NSAIDs, to reduce the blood pressure response to angiotensin-converting enzyme inhibitors. A more detailed discussion of the chemical, pharmacological, pharmacokinetic, and clinical aspects of celecoxib is available (81). [Pg.1482]

Angiotensin-converting enzyme (ACE) inhibitors, angiotensin-11 receptor blockers (ARBs), P-blockers, and calcium channel blockers are not dosed in the clinical setting using pharmacokinetic equations. The clinical use and selection of a drug within a class of medications is determined, in part, on differences in pharmacokinetic parameters. Eor example, metoprolol is commonly used in patients with renal disease because it is metabolized in the liver. Atenolol is avoided because it is renally eliminated. Select pharmacokinetic parameters for ACE inhibitors, ARBs, P-blockers, and calcium channel blockers are listed in Tables 8.11 through 8.13. [Pg.163]

AIIRAs do not inhibit ACE (kininase II, the enzyme that converts angiotensin I to angiotensin II and degrades bradykinin), nor do they bind to or block other hormone receptors or ion channels known to be important in cardiovascular regulation. Pharmacokinetics ... [Pg.591]


See other pages where Angiotensin-converting enzyme pharmacokinetics is mentioned: [Pg.509]    [Pg.265]    [Pg.79]    [Pg.715]    [Pg.382]    [Pg.1698]    [Pg.353]    [Pg.666]    [Pg.1291]    [Pg.874]   


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