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Ten most important things to learn from the ACCF/AHA 2011 expert consensus document on hypertension in the elderly.
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PMID:  21991999     Owner:  NLM     Status:  MEDLINE    
The American College of Cardiology Foundation/American Heart Association 2011 Expert Consensus Document on Hypertension in the Elderly has been published in the Journal of the American College of Cardiology and in Circulation, and will be published in the Journal of the American Society of Hypertension and the Journal of Geriatric Cardiology. This document has also been developed in collaboration with the American Academy of Neurology, the American Geriatrics Society, the American Society of Preventive Cardiology, the American Society of Hypertension, the American Society of Nephrology, the Association of Black Cardiologists, and the European Society of Hypertension. The present article is a short summary emphasizing the 10 most important things to learn from this document.
Wilbert S Aronow; Maciej Banach
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Publication Detail:
Type:  Journal Article     Date:  2011-10-13
Journal Detail:
Title:  Blood pressure     Volume:  21     ISSN:  1651-1999     ISO Abbreviation:  Blood Press.     Publication Date:  2012 Feb 
Date Detail:
Created Date:  2012-01-23     Completed Date:  2012-05-28     Revised Date:  2013-07-23    
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Nlm Unique ID:  9301454     Medline TA:  Blood Press     Country:  England    
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Languages:  eng     Pagination:  3-5     Citation Subset:  IM    
Cardiology Division, Department of Medicine, New York Medical College, Valhalla, New York 10595, USA.
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MeSH Terms
Aged, 80 and over
Antihypertensive Agents / therapeutic use*
Blood Pressure / drug effects
Consensus Development Conferences as Topic
Hypertension / complications,  drug therapy*,  physiopathology
Practice Guidelines as Topic
Randomized Controlled Trials as Topic
Stroke / etiology,  physiopathology,  prevention & control*
United States
Reg. No./Substance:
0/Antihypertensive Agents

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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Journal Information
Journal ID (nlm-ta): Blood Press
Journal ID (iso-abbrev): Blood Press
Journal ID (publisher-id): sblo
ISSN: 0803-7051
ISSN: 1651-1999
Publisher: Informa Healthcare
Article Information
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© 2012 Informa Healthcare
Received Day: 27 Month: 1 Year: 2012
Accepted Day: 29 Month: 4 Year: 2012
Print publication date: Month: 7 Year: 2012
Electronic publication date: Day: 05 Month: 7 Year: 2012
Volume: 21 Issue: Suppl 1
First Page: 3 Last Page: 10
ID: 3469239
PubMed Id: 21991999
DOI: 10.3109/08037051.2012.690615

Long-acting dihydropyridine calcium-channel blockers and sympathetic nervous system activity in hypertension: A literature review comparing amlodipine and nifedipine GITS
Corey B. Toal1
Peter A. Meredith2
Henry L. Elliott3
1Department of Pharmacology, University of Toronto, Toronto, Canada
2University of Glasgow, Glasgow, UK
3University of Strathclyde, Glasgow, UK
Correspondence: Correspondence: Corey B. Toal, Department of Pharmacology, University of Toronto, 1 Kings College Circle, Toronto, Ontario, Canada. Tel: 416–209–0923. E-mail:


Calcium-channel blockers (CCBs), comprise three distinct subgroups: benzothiazepines (e.g. diltiazem), dihydropyridines (e.g. amlodipine, nifedipine) and phenylalkylamines (e.g. verapamil). Despite this diversity, they are often referred to as a single, homogeneous class of pharmacological agents. Furthermore, even within the dihydropyridine group, there are numerous drugs and formulations (e.g. nifedipine capsules, retard, gastrointestinal therapeutic system: GITS) with different pharmacokinetic profiles, clinical uses and responses, and different dosing requirements.

Despite these various pharmacokinetic differences, arterial vasodilatation is the fundamental response to calcium-channel blockade with a dihy-dropyridine CCB. Peripheral arterial vasodilatation leads to a reduction in blood pressure and coronary artery vasodilatation leads to increased blood flow to the myocardium. However, it has long been known that potent arterial vasodilators evoke a barorecep-tor-mediated reflex increase in heart rate that is mediated via the sympathetic nervous system. This holds for both arterial vasodilators, such as nifedipine and hydralazine (1), and for mixed arterio-venous dilators such as nitroglycerin (2). Thus, the positive consequences of arterial vasodilatation may be compromised by activation of the sympathetic nervous system and an increase in heart rate.

Insights into the balance between these positive and negative effects became apparent in the results of the early studies with nifedipine in its immediate release formulation: two clinical outcome studies indicated that in patients with unstable angina (3) and post-myocardial infarction (4), the administration of nifedipine, as a potent arterial vasodilator, did not lead to a clear reduction in morbidity and mortality. At the time, this appeared counter-intuitive because coronary vasodilatation in both these conditions would be expected to increase oxygen delivery to the myocardium and benefit the patients, as would the reduction in cardiac work through the reduction in afterload. However, in hindsight, reflex sympathetic activation, catecholamine release and increased heart rate would be likely to have offset the expected beneficial effect.

In a later review, Grossman & Messerli (5) suggested that rapid-onset, short-acting dihydropyridine CCBs evoked sympathetic activation, whether administered acutely or over several weeks. In contrast, long-acting dihydropyridine CCBs did not evoke the same response. However, this is an over-simplification: for example, the once-daily ER formulation of the dihydropyridine drug felodipine has been shown to elevate plasma catecholamines (a marker of sympathetic activation) and result in less left ventricular regression in hypertensive patients compared with either enalapril or nifedipine GITS (6,7).

Despite obvious differences between drugs, between classes or subgroups or formulations, CCBs are often indiscriminately grouped together. They are often summarized as a single entity in reviews of outcome trials and when reviewed by formulary committees and by funding organizations. This raises obvious questions about the most appropriate method of considering the interchangeability of different CCBs and, for this reason, we decided to conduct a detailed review of the literature on two of the most commonly used dihydropyridine CCBs, amlodipine and nifedipine GITS, with specific regard to their effects on sympathetic activation.

Literature review

The MEDLINE (Pubmed), Embase, Derwent Drug File, Biosis and Science Citation Index databases were searched for articles published between 1990 and April 2011 on amlodipine and nifedipine using the terms sympathetic nervous system, sympathetic response, sympathetic nerve activity, noradrenaline, norepinephrine, heart rate, hypertension. We included only articles published in the English language. If a study was published in more than one journal, efforts were made only to include the data once from whichever article was most complete in study details and data. The primary focus was on full manuscript publications and not abstracts. However, if an abstract was published but a full paper was not subsequently found, the abstract was used if there were data on number of patients, dose of drug, duration of treatment and relevant measurement values. More than 1500 articles were screened and only those in which treatment lasted for at least 1 week were included in the analysis.

Indices of sympathetic nervous system activity

The following measurements of sympathetic nervous system activity/sympathetic activation were evaluated:

  • (1)  plasma norepinephrine (noradrenaline) concentrations;
  • (2)  muscle sympathetic nerve activity recordings;
  • (3)  power spectral analyses of low-frequency and high-frequency activity.

All plasma concentration values for norepineph-rine were converted to pg/ml and changes were calculated as percentage (%) values. Sympathetic activation values were included for patients at rest as distinct from those stimulated by mental stress, handgrip, standing or cold pressor tests.

Background details

Generally, data were reported for patients in the supine or sitting position. For the blood pressure measurements, office- or clinic-based values are incorporated and average daytime values if ambulatory blood pressure readings were used. If the final blood pressure, heart rate or other measurement was not given as an absolute value but as a change from baseline, the end of measurement value was calculated by simply adding the mean change value to the initial/baseline value. To make allowances for different baseline values, different study designs, different methodologies etc., percentage changes from baseline to the end time point have been calculated. If measurements were made at multiple time points within one published study, the longest duration of treatment was chosen and if multiple doses were reported, or dose titration occurred, the final dose of drug or the most-used dose is reported.


Only one study permitted a direct statistical comparison (8). It was adjudged that formal statistical testing was not otherwise appropriate because of wide variability in the results and because of significant differences in methodologies, study characteristics and relatively small study numbers. Thus, summary statistics (means, standard error and percentage change) were used to make comparisons between the drugs.

Plasma norepinephrine

Measurement of plasma norepinephrine concentrations was the most commonly reported index of sympathetic activity and activation. Twenty-three (23) studies were identified for amlodipine and 14 (14) for nifedipine GITS. For amlodipine, 698 patients were evaluated with an overall mean age of 56 years (Table I). Corresponding mean values for nifedipine GITS were 291 patients and 57 years (Table II). There was considerable variability in the plasma norepinephrine results in that the changes from baseline ranged from—21.4% to 55.6% with amlodipine and from—3.1% to 58.9% with nifedipine GITS.

The changes in blood pressure (BP) and heart rate were similar with the two drugs. With amlodipine, systolic blood pressure (SBP) decreased by 10.2±0.9%, diastolic blood pressure (DBP) by 10.4±0.8% and heart rate increased by 0.6±0.8% (Table I). With nifedipine GITS, the respective changes were 10.9±1.7%, 12.0±1.6% and 0.7±0.9% (Table II).

In summary, plasma norepinephrine increased by 21.7±4.3% after amlodipine and by 17.1±5.7% after nifedipine GITS (Figure 1).

Muscle sympathetic nerve activity

Measurement of muscle (peroneal nerve) sympathetic activity was the second most commonly used method and was employed in five amlodipine studies and in one study with nifedipine GITS. In the amlodipine studies, a total of 70 patients with an average age of 52 years were evaluated (Table III). For nifedipine GITS, the single small study split the 18 patients into older and younger groups for evaluation but the overall mean age was similar at 56 years (Table III).

The changes in SBP, DBP and heart rate were 8.4±1.0%, 6.7±1.0% and 0.4±2.2%, respectively, in the amlodipine studies and the corresponding values were 3.8±3.0%, 4.5±3.5% and 3.0±0.1% in the nifedipine studies.

In summary, the increase in muscle sympathetic nerve activity was 21.4±8.5% for amlodipine and 6.7±1.8% for nifedipine GITS (Figure 2).

Power spectral analysis

This methodology involves continuous measurement of the ECG to tease out R–R interval variations using fast Fourier transformation and autoregressive algorithms (9). The low-frequency component of the power spectrum is an indicator of sympathetic nerve activity to the heart and high-frequency activity is a measure of parasympathetic activity. Ten studies on amlodipine in hypertensive patients looked at these measures. The average age of the 180 patients studied was 54 years (Table IV). There were no such studies with nifedipine GITS.

In the amlodipine-treated patients, the decreases in SBP, DBP and heart rate were 13.5±1.8%, 10.8±1.0% and 1.0±1.3% (Table IV). The low-frequency component of the power spectrum decreased by 3.3±7.5%, the high-frequency component increased by 6.2±6.6% and the ratio of low to high frequency increased by 11.9±12.6% (Figure 3).


The activity of the sympathetic nervous system is essential for the moment-to-moment regulation of the cardiovascular system but “overactivity” has been implicated in both the genesis of, and the complications of, cardiovascular disease (10,11). With regard to treatment effects, specifically with dihydropyridine CCBs, it has been reported that the short-acting and long-acting drugs have distinctly different effects on the sympathetic nervous system (5). This conclusion was in complete accord with the findings in the seminal studies of Kleinbloesem et al. (12,13), which demonstrated that the “rate of drug delivery” was critical for determining the rate of onset of vasodilatation and hence the reflex effects expressed via the sympathetic nervous system. Thus, formulations of dihydropyridine CCBs, which result in a steep rise in plasma drug concentrations, have been shown to activate the sympathetic nervous system, e.g. nife-dipine capsule, nifedipine retard or felodipine (7,8,1214). In summary, sympathetic activation is typically seen with short-acting dihydropyridine CCBs but the fundamental factor is rapid-onset vasodilatation.

In the earlier review by Grossman & Messerli (5), long-acting agents were indiscriminately grouped together. This present overview compares the evidence derived in studies of the two established long-acting, once-daily dihydropyridine CCBs, which have the greatest volume of clinical outcome evidence: amlodipine an agent with an intrinsically long pharmacokinetic elimination half-life and nifedipine GITS, a high-tech osmotic delivery system, which confers extended release characteristics (15).

Unfortunately, there is only one study that directly compares amlodipine and nifedipine GITS: the conclusion of this single study was that chronic treatment with amlodipine was associated with sympathetic activation, whereas no such activation occurred with nifedipine GITS. This finding is consistent with the overall trend in this present analysis albeit there was no statistical significance. However, the changes in baseline for plasma norepinephrine do not appear to be directly related to the blood pressure lowering effect, since the blood pressure decreases were very similar between the two drugs with, if anything, a marginally greater decrease with nifedipine GITS. Furthermore, the heart rate changes were comparable with the two drugs at approximately 0.6 beats/min.

Thus, the main finding of this overview is that amlodipine (despite its “positive” profile in clinical outcome studies) caused a small but significant activation of the sympathetic nervous system, as assessed by multiple markers. It is also noteworthy that, for measurements of plasma norepinephrine and assessment of muscle sympathetic activation, the percentage increases are coincidentally almost identical (i.e. 21.7% and 21.4%, respectively). In turn, the ratio of low to high frequency from the power spectral analysis suggests that the sympathetic activation component overall is greater than the parasympathetic component after amlodipine administration. Therefore, there is consistency in three different surrogate measures for sympathetic activation, suggesting that amlodipine increases activity of the sympathetic nervous system in hypertensive patients.

A detailed explanation for the apparent differential effects of amlodipine and nifedipine GITS on the sympathetic nervous system is not readily apparent. However, in studies of spontaneously hypertensive rats (SHR), Huang & Leenen (16) concluded that, even during chronic amlodipine administration, there was a balance between peripheral effects and central effects, whereby the plasma concentration of drug might influence the activation of the sympathetic nervous system. Similar results were obtained in a study with nifedipine in SHR (17). However, a slow peripheral intravenous infusion of nifedipine in SHR resulted in a sympatho-inhibitory response–decrease in blood pressure, renal sympathetic nerve activity and heart rate. The GITS osmotic delivery system with nife-dipine may be thought to mimic more closely a slow infusion of drug (relative to other formulations e.g. capsules, Retard) and explain to some degree the more neutral effects seen with nifedipine GITS compared with previous formulations. Taken together, these studies with amlodipine and nifedipine GITS suggest that BP reduction and the effects on the sympathetic nervous system reflect a dynamic equilibrium between central and peripheral effects, which, in turn, are dependent on peripheral (plasma) and central (central nervous system) concentrations of drug.

Notwithstanding the above observations and discussion, the results of this overview must be taken in proper context. The data are compiled from studies spanning some 20 years with patients of varying durations of hypertension, severity of disease, baseline blood pressures, conditions for sampling or measurements, time of day, body posture, dose of drug, age of patient etc. Moreover, no formal statistical analyses were conducted because of varying methodologies and study characteristics, and widely varying results. All of these are potentially complicating and confounding factors when trying to compare drugs. Ideally, a study comparing the two drugs in a head-to-head manner with proper randomization and assessment should provide more robust data. To date, only one such study was found, that by de Cham-plain et al. (8). In that study, although amlodipine did not result in a transient rise in plasma norepi-nephrine after either acute or chronic dosing, administration for 6 weeks was reported to cause a 50% increase in the overall basal concentration of plasma norepinephrine. This was not observed with nife-dipine GITS.

Chronic activation of the sympathetic nervous system has been implicated in the pathogenesis of hypertension and its cardiovascular complications. However, both amlodipine and nifedipine GITS have positive outcome data in the treatment of hypertensive patients (i.e. ALLHAT, INSIGHT respectively (18,19)). This suggests that there is a balance between the benefits of lowering blood pressure and the potentially adverse consequences of sympathetic activation. In practice, therefore, effective BP reduction may be more important than modest sympathetic activation. There are additional considerations, the most obvious of which is that many patients require multiple drugs to manage their blood pressure and the interaction of these other drugs in conjunction with the CCBs may have some counterbalancing effect. Overall, despite the view fostered by the major hypertension treatment guidelines, it is apparent that the dihydropyri-dine CCBs cannot be considered a homogenous group of compounds. Furthermore, even two long-acting once-a-day drugs like amlodipine and nife-dipine GITS, with similar clinical profiles, may have both qualitatively and quantitatively different effects on the sympathetic nervous system.

The publication of this article has been supported by an unrestricted grant from Bayer AG.

Declaration of interest

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.

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[Figure ID: fig1]
Figure 1 

The effects of amlodipine and nifedipine gastrointestinal therapeutic system (GITS) on systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and plasma norepinephrine (NE) when the drug is given over weeks of treatment. This figure is based on the mean percentage changes from Tables I and II for all the studies cited.

[Figure ID: fig2]
Figure 2 

The effects of amlodipine on systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR) and muscle sympathetic nerve activity (MSA) when the drug is given over weeks of treatment. This figure is based on the mean percentage changes from Table III for all the studies cited.

[Figure ID: fig3]
Figure 3 

The effects of amlodipine on systolic blood pressure (SBP), diastolic blood pressure (DBP), heart rate (HR), low frequency (LF), high frequency (HF) and the ratio of low to high frequency (LF/HF) of the power spectrum when the drug is given over weeks of treatment. This figure is based on the mean percentage changes from Table IV for all the studies cited.

[TableWrap ID: tbl1] Table I 

Studies on amlodipine reporting plasma norepinephrine.

Referencea Year n Mean age (years) Dose (mg) Time interval (weeks) %Δ in SBP %Δ in DBP %Δ in HR %Δ in NE
Lopez et al. (20) 1990 12 61 2.5–10 4 –8.1 –8.9 35.1
Donati et al. (21) 1992 10 47 5 8 –11.3 –9.3 –5.6 –8.7
Leenen and Fourney (22) 1996 17 55 10 26 –13.3 –12.7 –11.1
Sasaguri et al. (23) 1997 8 5 1 –13.2 –8.8 1.2 3.0
Hamada et al. (24) 1998 16 60 5 4 –10.5 –7.2 –1.4 –21.4
de Champlain et al (8) 1998 22 55 10 6 –10.0 –12.6 8.0 55.6
Sakata et al. (25) 1999 24 63 10 12 –17.7 –20.2 0.0 18.9
Malamani et al. (26) 1999 60 10 12 41.7
Spence et al. (27) 2000 24 47 10 4 –7.9 –8.9 4.1 27.7
Fogari et al. (28) 2000 15 55 10 24 –11.9 –13.7 1.4 34.9
Lefrandt et al. (29) 2001 145 51 5 8 –9.8 –9.0 1.5 23.2
Struck et al. (30) 2002 18 56 5 1 –9.1 –5.3 6.0 33.7
Eguchi et al. (31) 2002 46 69 10 8 –17.3 –10.9 –2.9 23.8
Binggeli et al. (32) 2002 14 58 5 8 –9.7 –9.6 –4.6 47.1
Ohbayashi et al. (33) 2003 37 68 5 26 –1.4 –1.3 0.0 13.0
Malacco et al. (34) 2004 46 57 10 12 –9.8 –12.6 2.7 15.2
Karas et al. (35) 2005 22 57 10 8 –14.3 –12.0 48.8
Leenen et al. (36) 2006 29 41 5 8 –4.4 –15.1 19.3
Leenen et al. (36) 2006 37 67 5 8 –0.7 –11.4 7.4
Ruzicka et al. (37) 2007 10 42 5 6 –4.6 –4.4 –2.7 18.6
de Champlain et al. (38) 2007 23 57 10 8 –12.8 –12.4 1.4 38.2
Larochelle et al. (39) 2008 42 58 10 8 –12.3 –11.6 38.1
Sanjuliani et al. (40) 2002 21 47 10 26 –15.2 –3.6
Total 698
Mean 55.8
Mean % change –10.2 –10.4 0.6 21.7
SE 0.94 0.83 0.78 4.27

SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; NE, norepinephrine; %Δ, percentage change.

aEach reference is an independent study published reporting on the relevant parameters indicated with % changes calculated on the group means.

[TableWrap ID: tbl2] Table II 

Studies on nifedipine gastrointestinal therapeutic system reporting plasma norepinephrine.

Referencea Year n Mean age (years) Dose (mg) Time interval (weeks) %Δ in SBP %Δ in DBP %Δ in HR %Δ in NE
Frohlich et al. (41) 1991 10 52 65 8 –12.6 –10.9 5.7 –3.1
Phillips et al. (42) 1992 16 56 30–150 52 –28.0 –27.0 –3.7 –1.5
Halperin et al. (43) 1993 12 53 30–90 4 –8.3 –11.1 –2.4 16.8
DeQuattro and Lee (44) 1997 23 66 30–120 12 –12.2 –10.2 40.0
de Champlain et al. (8) 1998 22 51 30–60 6 –8.6 –10.9 0.0 0.0
James et al. (45) 1999 14 70 30–60 6 –12.3 –12.8 –3.0 –0.5
Pellizer et al. (46) 2001 8 57 60 6 –7.5 –8.7 –1.3 58.9
Diamond et al. (47) 2001 15 46 30–120 26 –17.4 –18.2 1.2 0.0
Leenen et al. (7) 2002 17 55 30 30 –9.9 –10.0 57.0
Fogari et al. (48) 2003 30 55 60 48 –13.2 –14.9 0.0 26.0
Ruzicka et al. (49) 2004 10 45 20 4 –0.8 –1.1 2.9 4.3
Ruzicka et al. (49) 2004 8 67 20 4 –6.8 –8.0 7.7 6.6
Fogari et al. (50) 2005 62 59 60 12 –9.8 –12.7 2.7 19.9
Brown and Toal (51) 2007 44 63 30 2 –6.0 –1.4 14.3
Total 291
Mean 56.8
Mean % change –10.9 –12.0 0.7 17.1
SE 1.68 1.60 0.94 5.68

SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; NE, norepinephrine; %Δ, percentage change.

aEach reference is an independent study published reporting on the relevant parameters indicated with %changes calculated on the group means.

[TableWrap ID: tbl3] Table III 

Studies on amlodipine and nifedipine gastrointestinal therapeutic system (GITS) reporting muscle sympathetic nerve activity.

Referencea Year n Mean age (years) Dose (mg) Time interval (weeks) %Δ in SBP %Δ in DBP %Δ in HR %Δ in MSA
 Calhoun (52) 1997 10 47 10 4 –9.6 –7.6 2.9 40.0
 Binggeli et al. (32) 2002 14 58 5 8 –9.7 –9.6 –4.6 6.1
 Struck et al. (30) 2002 18 56 5 1 –9.1 32.1
 Ruzicka et al. (37) 2007 10 42 5 6 –4.6 –4.4 –2.7 –3.9
 Dodt et al. (53) 2000 18 56 5 1 –9.1 –5.3 6.0 32.6
 Total 70
 Mean 51.8
 Mean % change –8.4 –6.7 0.4 21.4
 SE 0.97 1.04 2.19 8.54
Nifedipine GITS
 Ruzicka et al. (49) 2004 10 45 20 4 –0.76 –1.012 2.94 4.88
 Ruzicka et al. (49) 2004 8 67 20 4 –6.85 –8.05 3.08 8.51
 Total 18
 Mean 56
 Mean % change –3.81 –4.53 3.01 6.69
 SE 3.04 3.52 0.07 1.82

SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; MSA, muscle sympathetic nerve activity; %Δ, percentage change.

aEach reference is an independent study published reporting on the relevant parameters indicated with % changes calculated on the group means.

[TableWrap ID: tbl4] Table IV 

Studies on amlodipine reporting power spectral analysis.

Referencea Year n Mean age (years) Dose (mg) Time interval (weeks) %Δ in SBP %Δ in DBP %Δ in HR %Δ in LF %Δ in HF %Δ in LF/HF
Minami et al. (54) 1998 20 63 5 4 –7.43 –4.55 1.37 –1.38 –5.60 10.29
Hamada et al. (24) 1998 16 60 5 4 –10.49 –7.23 –1.45 –3.52 16.67 –12.50
Lucini et al. (55) 1999 19 54 5 8 –12.73 –11.58 4.29 –9.84
Siche et al. (56) 2001 18 8 8 –11.41 –62.00 –33.33
Sahin et al. (57) 2004 20 48 10 4 –28.74 –14.00 22.22 35.48 –10.34
Karas et al. (35) 2005 22 57 10 8 –14.29 –12.00 25.00 11.11 73.33
Bilge et al. (58) 2005 14 46 10 13 –11.11 –11.70 –1.22 –1.48 –2.17 0.76
Bilge et al. (58) 2005 14 46 10 26 –13.19 –13.83 –3.66 –2.31 –2.82 0.00
Linqvist et al. (59) 2007 14 59 10 6 –12.94 –9.89 6.06 –7.25 16.13 –26.47
de Champlain et al. (38) 2007 23 57 10 8 –12.84 –12.37 1.41 7.41 20.00 60.00
Total 180
Mean 54.4
Mean % change –13.52 –10.79 0.97 –3.31 6.16 11.88
SE 1.80 1.04 1.28 7.51 6.60 12.62

SBP, systolic blood pressure; DBP, diastolic blood pressure; HR, heart rate; LF, low frequency; HF, high frequency; LF/HF, ratio of low frequency to high frequency; %Δ, percentage change.

aEach reference is an independent study published reporting on the relevant parameters indicated with % changes calculated on the group means.

Article Categories:
  • Original Article

Keywords: Amlodipine, blood pressure, catecholamines, extended release, GITS, nifedipine, norepinephrine, sympathetic activation, sympathetic nerve activity.

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