Amlodipine

Burges, Roger A.; Dodd, Michael G.

doi:10.1111/j.1527-3466.1990.tb00427.x

Cited by 27 publications

(11 citation statements)

References 57 publications

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“…These features permit once-dailv dosing and avoid repeated peaks and troughs in the serum con centration profile. Amlodipine also demon strates a slower onset of action than nifedi pine at the receptor site [5]. These characteris tics strongly suggest that initiation of amlodi pine therapy may be associated with a lower incidence of classical early vasodilator-related adverse effects compared with nifedipine.…”

Section: Introductionmentioning

confidence: 69%

Comparison of Early Side Effects with Amlodipine and Nifedipine Retard in Hypertension

Hosie¹,

Bremner²,

Fell³

et al. 1992

Cardiology

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The frequency and severity of adverse effects during the first 14 days of treatment with amlodipine (5 mg once daily), nifedipine retard (20 mg twice daily) or placebo were compared in a multicentre, three-way, cross-over study involving 97 patients with mild-to-moderate hypertension. All three groups of patients were well matched for age, sex and baseline blood pressure. Amlodipine and nifedipine retard produced highly significant and comparable reductions in blood pressure, indicating that the doses were therapeutically equivalent. The incidence of adverse effects considered to be definitely or probably related to nifedipine retard treatment (41%) was significantly higher than for placebo (16%, p < 0.01) or amlodipine (27%, p < 0.05). There were no significant differences in the incidence of vasodilator-related adverse effects between amlodipine and placebo. In contrast, headache, flushing and dizziness were reported more frequently by patients while on nifedipine retard than on placebo or amlodipine. The convenience of once-daily dosing, together with a lower incidence of adverse effects, with consequently fewer withdrawals from therapy, suggests that amlodipine has clinical advantages over nifedipine retard in the treatment of hypertension.

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Section: Introductionmentioning

confidence: 69%

Comparison of Early Side Effects with Amlodipine and Nifedipine Retard in Hypertension

Hosie¹,

Bremner²,

Fell³

et al. 1992

Cardiology

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show abstract

“…In fact nifedipine has a rapid onset of action and reaches peak plasma concentration within 30 min of administration with a short duration of action (half life = 1-2 h) (Croom and Wellington, 2006;Meredith and Reid, 1993). On the other hand, amlodipine has a long duration of action (half life 8-35 h) and reaches peak plasma concentration between 6 and 8 h with a slow onset of action (Burges and Dodd, 1990;Nayler and Gu, 1991). Since both antiemetics were administered 30 min prior to the administration of the discussed emetogens, it is likely that amlodipine may not have had sufficient time to reach its sites of action thus leading to lower potency.…”

Section: Discussionmentioning

confidence: 96%

Broad-spectrum antiemetic efficacy of the l-type calcium channel blocker amlodipine in the least shrew (Cryptotis parva)

Zhong

Chebolu

Darmani

2014

Pharmacology Biochemistry and Behavior

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“…34,35 On the other hand, amlodipine has a long duration of action (half life=8-35 h) and reaches peak plasma concentration between 6 and 8 hour with a slow onset of action. 36,37 Since both antiemetics were administered 30 min prior to the administration of the discussed emetogens, it is likely that amlodipine may not have had sufficient time to reach its sites of action, thus having lower potency. In addition, the positively charged amlodipine associates more slowly with the l-type Ca 2+ channel, which can lead to a more gradual onset of antagonism.…”

Section: Antiemetic Potential Of Ltcc Blockersmentioning

confidence: 99%

Role of Calcium in Vomiting: Revelations from the Least Shrew Model of Emesis

Darmani

Zhong²

2015

Gastro Open J

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Citation-ATPase inhibitor) cause vomiting in the least shrew, whereas blockade of LTCC by corresponding antagonists (nifedipine or amlodipine) not only provide broad-spectrum antiemetic activity against diverse emetogens including agonists of 5-HT 3 (e.g. 5-HT or 2-Me-5-HT)-, NK 1 (GR73632)-, D 2 (apomorphine or quinpirole)-, and M 1 (McN-A343)-receptors, but can also potentiate the antiemetic efficacy of well-established antiemetic palonosetron against the non-specific emetogen, cisplatin. The transmission of emesis signals in the gastrointestinal tract and brainstem is crucially dependent on Ca 2+ channels in neurons. In this review, we will examine the current knowledge on the role of Ca 2+ channels and Ca 2+-dependent signaling pathways in the perception and modulation of emesis.

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Amlodipine

Cited by 27 publications

References 57 publications

Comparison of Early Side Effects with Amlodipine and Nifedipine Retard in Hypertension

Comparison of Early Side Effects with Amlodipine and Nifedipine Retard in Hypertension

Broad-spectrum antiemetic efficacy of the l-type calcium channel blocker amlodipine in the least shrew (Cryptotis parva)

Role of Calcium in Vomiting: Revelations from the Least Shrew Model of Emesis

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