The 24-hour ambulatory blood pressure profile with verapamil.

Gould, Brian A.; Mann, Stewart; Kieso, H; Subramanian, Vijay; Raftery, Edward B.

doi:10.1161/01.cir.65.1.22

Cited by 131 publications

(30 citation statements)

References 25 publications

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“…The results of this study show that nicardipine, 30 mg three times daily is an effective hypotensive agent, comparable with standard doses of /?-adrenoceptor blockers (Asplund, 1981), thiazides (Multicentre Diuretic Co-operative Study Group, 1981), verapamil (Gould et al, 1981), and nifedipine (Pederson et al, 1979). In an open study Takabatake et al (1982) obtained a reduction in mean systolic/diastolic blood pressure of 17.8/14.2 mm Hg after 4 weeks of treatment with nicardipine 10 mg three times daily -one third of the dose used in the present study.…”

Section: Discussionmentioning

confidence: 58%

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Asplund¹

1985

Brit J Clinical Pharma

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Fifty patients with mild essential (primary) hypertension entered a double‐blind, parallel‐group study with either nicardipine 30 mg three times daily or placebo, randomly assigned as monotherapy for 6 weeks. At the end of 6 weeks, the nicardipine‐treated group had a statistically significant reduction in mean supine systolic/diastolic pressure of 21.2/15.0 mm Hg (P less than 0.001) compared with the nonsignificant reduction of 0.7/2.9 mm Hg in the placebo‐treated group. The difference in mean response between the nicardipine‐ and placebo‐ treated groups was significant (P less than 0.001). In the nicardipine‐ treated group, the reduction in mean standing systolic/diastolic blood pressure, 17.9/13.8 mm Hg, was significant (P less than 0.001), whereas in the placebo‐treated group the change was +3.0/‐1.5 mm Hg. The difference between the two treatment groups was significant (P less than 0.001). In both treatment groups, changes in pulse rate were minor, and there was no evidence of tachyphylaxis occurring with nicardipine. Adverse experiences were minor in all cases except for one patient with muscle pain during treatment with nicardipine. Patients who received nicardipine showed a mean increase of 52% in plasma renin activity (PRA) after 6 weeks (P less than 0.01). Initial basal or stimulated PRA did not correlate with blood pressure reduction on nicardipine. Nicardipine 30 mg three times daily is a well‐tolerated and effective antihypertensive agent.

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Section: Discussionmentioning

confidence: 58%

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Asplund¹

1985

Brit J Clinical Pharma

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“…[17][18][19][20]31,32 The retrospective Syst-Eur 25 and HOPE 33 outcome trials show that evening administration of nitrendipine and ramipril impacts sleep-time blood pressure by converting the 24-h blood pressure pattern to a dipper pattern and decreasing CVD risk in the HOPE study. The CONVINCE trial 34,35 did not show a chronotherapy benefit, but the MAPEC trial 36 results suggest that night time dosing is beneficial.…”

Section: Perspectivesmentioning

confidence: 99%

Fixed-combination of amlodipine and diuretic chronotherapy in the treatment of essential hypertension: improved blood pressure control with bedtime dosing—a multicenter, open-label randomized study

et al. 2011

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Previous studies have demonstrated that individual anti-hypertension medications have different effects when administered in the morning vs. the evening. However, the impact of administration timing on fixed combinations of anti-hypertensive medications on blood pressure control is still unknown. In the present study, we examined the administration time-dependent effects of a fixed combination of amlodipine and diuretics (amlodipine complex) on blood pressure in hypertensive subjects. Eighty patients from Chongqing City were enrolled in this study. Subjects were randomly assigned to receive a single pill (amlodipine complex, each tablet containing amlodipine 5 mg and hydrochlorothiazide 25 mg), either in the morning (0800 hours, n¼40) or at bedtime (2200 hours, n¼40). Blood pressure was measured by ambulatory monitoring every 20 min during the day and every 30 min at night for 24 consecutive hours before and after the 12 weeks of treatment. Following treatment, the 24-h mean systolic and diastolic blood pressures were reduced significantly in both the morning and bedtime groups. However, the morning blood pressure surge was reduced to a greater degree in the bedtime group. In addition, the nocturnal blood pressure and the 24 h mean blood pressure were lower in the bedtime group. More patients converted from having a non-dipper to dipper blood pressure in the bedtime group. These findings confirm that amlodipine complexes have different efficiencies depending on treatment time. Administration of amlodipine complexes at bedtime could optimize the anti-hypertensive effect by augmenting blood pressure-lowering effects, increasing the diurnal/nocturnal ratio of blood pressure, normalizing the blood pressure pattern and minimizing the morning blood pressure surge.

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“…The calcium channel blocker verapamil ( Figure 1A), which is commonly used to control hypertension, chest pain and arrhythmia [15][16][17][18][19], functions as a substrate and an inhibitor of the transporter [7]. From results of in vitro studies, the drug is known to activate Pgp-coupled ATP-hydrolysis [20].…”

Section: Introductionmentioning

confidence: 99%

Unravelling the complex drug–drug interactions of the cardiovascular drugs, verapamil and digoxin, with P-glycoprotein

2016

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SynopsisDrug-drug interactions (DDIs) and associated toxicity from cardiovascular drugs represents a major problem for effective co-administration of cardiovascular therapeutics. A significant amount of drug toxicity from DDIs occurs because of drug interactions and multiple cardiovascular drug binding to the efflux transporter P-glycoprotein (Pgp), which is particularly problematic for cardiovascular drugs because of their relatively low therapeutic indexes. The calcium channel antagonist, verapamil and the cardiac glycoside, digoxin, exhibit DDIs with Pgp through non-competitive inhibition of digoxin transport, which leads to elevated digoxin plasma concentrations and digoxin toxicity. In the present study, verapamil-induced ATPase activation kinetics were biphasic implying at least two verapamil-binding sites on Pgp, whereas monophasic digoxin activation of Pgp-coupled ATPase kinetics suggested a single digoxin-binding site. Using intrinsic protein fluorescence and the saturation transfer double difference (STDD) NMR techniques to probe drug-Pgp interactions, verapamil was found to have little effect on digoxin-Pgp interactions at low concentrations of verapamil, which is consistent with simultaneous binding of the drugs and non-competitive inhibition. Higher concentrations of verapamil caused significant disruption of digoxin-Pgp interactions that suggested overlapping and competing drug-binding sites. These interactions correlated to drug-induced conformational changes deduced from acrylamide quenching of Pgp tryptophan fluorescence. Also, Pgp-coupled ATPase activity kinetics measured with a range of verapamil and digoxin concentrations fit well to a DDI model encompassing non-competitive and competitive inhibition of digoxin by verapamil. The results and previous transport studies were combined into a comprehensive model of verapamil-digoxin DDIs encompassing drug binding, ATP hydrolysis, transport and conformational changes.

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The 24-hour ambulatory blood pressure profile with verapamil.

Cited by 131 publications

References 25 publications

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Nicardipine hydrochloride in essential hypertension‐a controlled study.

Fixed-combination of amlodipine and diuretic chronotherapy in the treatment of essential hypertension: improved blood pressure control with bedtime dosing—a multicenter, open-label randomized study

Unravelling the complex drug–drug interactions of the cardiovascular drugs, verapamil and digoxin, with P-glycoprotein

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