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Of nifedipine

Po adrninistered nifedipine is almost completely absorbed. The onset of action is 20 min and peak effects occur at 1—2 h. The principal route of elimination is through hepatic metaboHsm by oxidation to hydroxycarboxyHc acid and the corresponding lactone. These metaboHtes are pharmacologically inactive. Almost 70—80% of dmg is eliminated in the urine during the first 24 h. About 15% is excreted in the feces. The elimination half-life of nifedipine is about 1—2.5 h (1,98,99). Frequency of occurrence of side effects in patients is about 17% with about 5% requiring discontinuation of therapy (1,98,99). [Pg.126]

FIGURE 17.25 The structures of nifedipine and ryanodine. Nifedipine binds with high affinity to the Ca" -release channels of t-tubules. Ryanodine binds with high affinity to the Ca" channels of SR terminal cisternae. [Pg.555]

Fast DHP-induced lowering of blood pressure results in compensatory sympathetic activation and a subsequent increase in heart rate and cardiac oxygen demand. This unfavorable effect has been mainly associated with the use of short-acting DHPs, such as nonretarded formulations of nifedipine, nitrendipine, or... [Pg.298]

Neural networks have also been used in Slovenia, to model the release characteristics of diclofenac [52] in China, to study release of nifedipine and nomodipine [53] and in Yugoslavia to model the release of aspirin [54], More recently, work in this area has been extended to model osmotic pumps in China [55] and enteric coated tablets in Ireland [56],... [Pg.693]

The performance of this system is shown in Figure 17 for the release of nifedipine from the GITS system [47], The reproducibility of the release rates is remarkable. Also note that the fractions released over time from three separate doses are basically superimposable. It should also be noted that these systems have an inherent delay in the onset of drug delivery which arises from the time required to build up a sufficient hydrostatic pressure to permit release of the gel that is formed within the tablet during delivery. Figure 18 shows the comparison of the in vitro and in vivo cumulative fraction released for the 30 mg system. Clearly, the in vitro performance is mirrored in the in vivo data. [Pg.448]

Short-acting nifedipine may rarely cause an increase in the frequency, intensity, and duration of angina in association with acute hypotension. This effect may be obviated by using sustained-released formulations of nifedipine or other dihydropyridines. Other side effects of dihydropyridines include dizziness, flushing, headache, gingival hyperplasia, and peripheral edema. Side effects due to vasodilation such as dizziness, flushing, head-... [Pg.133]

Nifedipine is a calcium-channel blocker of the dihydropyridine group. It relaxes smooth muscle and dilates both coronary and peripheral arteries by interfering with the inward displacement of calcium-channel ions through the active cell membrane. Unlike verapamil, nifedipine can be given with beta-blockers. Long-acting formulations of nifedipine are preferred in the long-term treatment of hypertension. [Pg.27]

Adalat is a proprietary preparation of nifedipine (a dihydropyridine calcium-channel blocker). [Pg.35]

The choice between calcium antagonists must take into account the differential effect of nifedipine versus verapamil or diltiazem on cardiac performance (see above). When p-blockers are given, the potential consequences of reducing cardiac contractility (withdrawal of sympathetic drive) must be kept in mind. Since vasodilating P2-receptors are blocked, an increased risk of vasospasm cannot be ruled out Therefore, monotherapy with p-blockers is recommended only in angina due to coronary sclerosis, but not in variant angina. [Pg.308]

Nicardipine Nicardipine, l,4-dihydro-2,6-dimethyl-4-(3-nitrophenyl)-methyl-2-[(methyl-phenylmethyl)-amino]ethyl ester 3,5-pirididincarboxylic acid (19.3.7), is synthesized in a manner analogous to the synthesis of nifedipine, the only difference being that in the Hantsch synthesis, two different )3-dicarbonyl compounds are used simultaneously with o-nitrobenzaldehyde. During this, one of these in the enamine form of acetoacetic ester is simultaneously used as an amine component. A heterocycUzation reaction is accomplished by reacting, the methyl ester of 8-aminocrotonic acid with the 2-methyl-2-benzyl-aminoethyl ester of acetoacetic acid [24-27]. [Pg.264]

The preparation of nifedipine and other simple symmetric analogs is very straightforward (Scheme 11.1). 4-Aryldihydropyridine-3,5-dicarboxylates are isolable intermediates... [Pg.162]

Hamet P, Gong L. Antihypertensive therapy debate contribution from the Shanghai Trial Of Nifedipine in the Elderly (STONE). J Hypertens Suppl 1996 14(4) S9-14. [Pg.222]

Diltiazem, a benzothiazepine, has a pharmacodynamic and side-effect profile that is intermediary between those of nifedipine and verapamil. Diltiazem is mostly used in the treatment of stable angina. It also displays antihypertensive activity, although it is not widely used in antihypertensive treatment. In certain countries diltiazem is used as an antiarrhyth-mic agent with the same type of applications as verapamil. [Pg.332]

Data on the effect of calcium antagonists on cardiovascular disease risks in patients with hypertension are available from one moderate-to-large scale randomized, placebo-controlled trial. In the Systolic Hypertension in Europe (Syst-Eur) trial, nitrendipine-based therapy produced an approximate 10/5 mmHg reduction in SBP-DBP in patients with systolic hypertension and a 42% reduction in the risk of stroke. Similar results were observed in two large, nonrandomized, placebo-controlled trials (with alternate treatment assignment), i.e. the Shanghai Trial of Nifedipine in the Elderly and the Systolic Hypertension in China (Syst-China) trial. [Pg.573]

Patients with malignant-accelerated hypertension can usually be managed by oral therapy. Patients who are seen in a nursing home or clinic, whose BP is found to be above some arbitrary danger level like a BP of 180/120 should not automatically be given nifedipine sublingually. Indiscriminate use of nifedipine sublingually could lead to a major catastrophe like myocardial infarction or cerebrovascular episodes. Nifedipine activates sympathetic response and leads to precipitous drops of blood pressure followed by rebound hypertension. [Pg.581]

Rashid TJ, Martin U, Clarke H, et al (1995) Factors affecting the absolute bioavailability of nifedipine. Br J Clin Pharmacol 40 51-58... [Pg.446]

D. The vasodilatory effects of nifedipine are largely restricted to arteries (and consequently the afterload). It does not alter venous tone (and thus preload) significantly. [Pg.223]

Given the seriousness of the reported adverse events and the lack of any clinical documentation attesting to a benefit, the use of nifedipine capsules for hypertensive urgencies or emergencies should be abandoned (JAMA 1996 276 1328-1331)... [Pg.869]

Self-medication of a MAOI-induced hypertensive crisis is controversial. In a hypertensive crisis the lack of access to medical services may lead to even greater complications. A small dose of medication taken as part of a larger plan to blunt the rise in blood pressure may prevent serious complications. However, headache is common, has multiple causes, and patients may not accurately identify a headache due to hypertension without a blood pressure check. In addition, selfadministration of nifedipine, especially sublingually, may result in needless and perhaps dangerous drops in blood pressure. [Pg.298]

Gengo F, Timko J, D Antonio J, et al Prediction of dosage of lithium carbonate use of a standard predictive method. J Clin Psychiatry 41 319-321, 1980 Geoffroy M, Mogilnicka E, Nielsen M, et al Effect of nifedipine on the shuttlebox escape deficit induced by inescapable shock in the rat. Eur J Pharmacol 154 277-283, 1988... [Pg.642]

Nifedipine is a dihydropyridine calcium channel modulator, often used in the treatment of hypertension and angina. CYP3A4, with a minor contribution from CYP3A5, is the principal enzyme involved in the metabolism of nifedipine (81). Smith et al. examined the effect of St. John s wort (900mg/day... [Pg.79]


See other pages where Of nifedipine is mentioned: [Pg.126]    [Pg.526]    [Pg.227]    [Pg.53]    [Pg.166]    [Pg.447]    [Pg.333]    [Pg.346]    [Pg.769]    [Pg.883]    [Pg.185]    [Pg.267]    [Pg.52]    [Pg.45]    [Pg.152]    [Pg.213]    [Pg.490]    [Pg.161]    [Pg.162]    [Pg.163]    [Pg.163]    [Pg.179]    [Pg.205]    [Pg.584]    [Pg.440]    [Pg.221]    [Pg.222]    [Pg.224]    [Pg.443]   
See also in sourсe #XX -- [ Pg.175 , Pg.176 , Pg.177 , Pg.178 , Pg.179 , Pg.180 , Pg.181 , Pg.182 ]




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Nifedipine

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