Influence of nifedipine coat-core and amlodipine on systemic arterial stiffness modulated by sympathetic and parasympathetic activity in hypertensive patients

Fukuda, Michinari; Masuda, Takashi; Ogura, Mariko; Moriya, Takuya; Tanaka, Keiji; Yamamoto, Kazuya; Ishii, Akira; Yonezawa, Ryusuke; Noda, Chiharu; Izumi, Tohru

doi:10.1038/hr.2009.18

Cited by 7 publications

(8 citation statements)

References 35 publications

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“…On the other hand, several previous studies reported that both once-daily L-type CCBs, nifedipine and amlodipine, lowered clinical BP effectively with minimal effects on clinical HR, and there were small differences between nifedipine and amlodipine in the extent to which each activates the sympathetic nervous system with an overall non-significant trend in favor of nifedipine, as estimated by plasma norepinephrine concentrations, power spectral analysis, muscle sympathetic nerve activity and norepinephrine spillover as markers of sympathetic nervous system activation [20,21]. …”

Section: Discussionmentioning

confidence: 99%

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

Kanaoka

Tamura

Wakui

et al. 2013

IJMS

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Ambulatory blood pressure (BP) and heart rate (HR) profile are proposed to be related to renal deterioration and cardiovascular complication in hypertension and chronic kidney disease (CKD). In this study, we examined the beneficial effects cilnidipine, a unique L/N-type calcium channel blocker (CCB), in addition to renin-angiotensin system inhibitors, on ambulatory BP and HR profile, as well as cardiorenal function in hypertensive CKD patients. Forty-five patients were randomly assigned to the cilnidipine replacement group (n = 21) or the control CCBs group (n = 24) during a 24-week active treatment period. Although clinical BP values were similar in the cilnidipine and control CCBs groups after the treatment period, the results of ambulatory BP monitoring showed that the 24-h and daytime systolic BP levels in the cilnidipine group were significantly lower compared with the control group after the study. Furthermore, the left ventricular mass index (LVMI) was significantly decreased in the cilnidipine group compared to the control group after the study (LVMI, 135.3 ± 26.4 versus 181.2 ± 88.4, p = 0.031), with a significant difference in the changes in the LVMI between the cilnidipine and control groups (change in LVMI, −12.4 ± 23.7 versus 26.2 ± 64.4, p = 0.007). These results indicate that cilnidipine is beneficial for the suppression of pathological cardiac remodeling, at least partly, via a superior improving effect on ambulatory BP profile compared with control CCBs in hypertensive CKD patients.

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Section: Discussionmentioning

confidence: 99%

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

Kanaoka

Tamura

Wakui

et al. 2013

IJMS

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“… 7 – 10 Chronic management of hypertension with nifedipine may interfere with remodeling of large arteries and decrease arterial stiffness. 11 The vascular protective effects of nifedipine therapy might be related to BP reduction and appear shortly after initiation of treatment. 12 Therefore, vascular protection by nifedipine is not restricted to a prolonged BP modulation.…”

Section: Introductionmentioning

confidence: 99%

Early intervention of long-acting nifedipine GITS reduces brachial–ankle pulse wave velocity and improves arterial stiffness in Chinese patients with mild hypertension: a 24-week, single-arm, open-label, prospective study

Zhang

Wang

et al. 2016

DDDT

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BackgroundNifedipine gastrointestinal therapeutic system (GITS) is used to treat angina and hypertension. The authors aimed to study the early intervention impact on arterial stiffness and pulse wave velocity (PWV) independent of its blood-pressure-(BP) lowering effect in mild hypertensive patients.MethodsThis single-center, single-arm, open-label, prospective, Phase IV study recruited patients with mild hypertension and increased PWV from December 2013 to December 2014 (N=138; age, 18–75 years; systolic blood pressure, 140–160 mmHg; diastolic BP, 90–100 mmHg; increased brachial–ankle pulse wave velocity [baPWV, ≥12 m/s]). Nifedipine GITS (30 mg/d) was administered for 24 weeks to achieve target BP of <140/90 mmHg. The dose was uptitrated at 60 mg/d in case of unsatisfactory BP reduction after 4 weeks. Primary study end point was the change in baPWV after nifedipine GITS treatment. Hemodynamic parameters (office BP, 24-hour ambulatory BP monitoring, and heart rate and adverse events) were evaluated at baseline and followed-up at 2, 4, 8, 12, 18, and 24 weeks.ResultsMajority of patients (n=117; 84.8%) completed the study. baPWV decreased significantly at 4 weeks compared with baseline (1,598.87±239.82 vs 1,500.89±241.15 cm/s, P<0.001), was stable at 12 weeks (1,482.24±215.14 cm/s, P<0.001), and remained steady through 24 weeks (1,472.58±205.01 cm/s, P<0.001). Office BP reduced from baseline to week 4 (154/95 vs 136/85 mmHg) and remained steady until 24 weeks. Nifedipine GITS significantly decreased 24-hour ambulatory BP monitoring (P<0.001) after 24 weeks from baseline. Mean arterial pressure and pulse pressure were lowered significantly after 4, 12, and 24 weeks of treatment (P<0.001). These changes in baPWV were significantly correlated with changes in systolic blood pressure, diastolic BP, and mean arterial pressure (P<0.05), but not with changes in pulse pressure (P>0.05). There were no other drug-related serious adverse events.ConclusionNifedipine GITS was considerably effective in reducing baPWV and BP, indicating improvement in arterial stiffness as early as 4 weeks.

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“…This workload was of moderate intensity and could be considered an ordinary workload tantamount to that carried out when people perform their ADLs, such as walking at a quick pace or walking up stairs. 12) We speculated that patients with muscle weakness had increased functional arterial stiffness and excessive BP elevation in their daily physical activities. The LVM increase was likely accelerated in these patients because they suffered frequently from pressure overload in ordinary ADLs.…”

Section: )mentioning

confidence: 99%

“…The change from ba-PWV at the resting phase to that at the recovery phase (ΔPWV) was calculated as an indicator of functional arterial stiffness, with a negative value indicating greater vascular compliance. 12) Plasma brain natriuretic peptide (BNP) was also measured as an indicator of left ventricular pressure overload. 23) Relative wall thickness (RWT) was also calculated as an indicator of LVH with left ventricular dilatation using the following formula: RWT = (IVSd + PWd)/LVDd.…”

Section: )mentioning

confidence: 99%

Muscle Weakness Is Associated With an Increase of Left Ventricular Mass Through Excessive Blood Pressure Elevation During Exercise in Patients With Hypertension

et al. 2017

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SummaryAutonomic imbalance in hypertension induces excessive blood pressure (BP) elevation during exercise, thereby increasing left ventricular mass (LVM). Although muscle weakness enhances autonomic imbalance by stimulating muscle sympathetic activity during exercise, it is unclear whether muscle weakness is associated with an increase of LVM in patients with hypertension. This study aimed to investigate the relationships between muscle weakness, BP elevation during exercise, and LVM in these patients. Eighty-six hypertensive patients aged 69 ± 8 years with controlled resting BP (ie, < 140/90 mmHg) were recruited. Plasma brain natriuretic peptide (BNP), left ventricular mass index (LVMI), and knee extension muscle strength were measured. Changes in plasma noradrenaline (NORA) and brachial-ankle pulse wave velocity (ba-PWV) were assessed before and after an ergometer exercise test performed at moderate intensity (ΔNORA and ΔPWV, respectively). A difference between baseline and peak systolic BP during the exercise test was defined as BP elevation during exercise (ΔSBP). Relationships between muscle strength, ΔNORA, ΔPWV, ΔSBP, BNP, and LVMI were analyzed, and significant factors increasing LVM were identified using univariate and multivariate regression analyses. Muscle strength was negatively correlated with ΔNORA (r = -0.202, P = 0.048), ΔPWV (r = -0.328, P = 0.002), ΔSBP (r = -0.230, P = 0.033), BNP (r = -0.265, P = 0.014), and LVMI (r = -0.233, P = 0.031). LVMI was positively correlated with ΔPWV (r = 0.246, P = 0.023) and ΔSBP (r = 0.307, P = 0.004). Muscle strength was a significant independent factor associated with LVMI (β = -0.331, P = 0.010). Our findings suggest that muscle weakness is associated with an increase of LVM through excessive BP elevation during exercise in patients with hypertension. ( 1-3) Hypertension-related LVM increase leads to the progression of left ventricular dysfunction, which can result in chronic heart failure.4) Left ventricular hypertrophy (LVH) is also known to be a strong risk factor for future cardiac events and mortality. 4) Therefore, the prevention of LVM increase is considered a promising therapeutic strategy, in addition to BP control, in patients with hypertension.Patients with hypertension have been known to exhibit an autonomic imbalance even in ordinary activities of daily living (ADL), which indicates elevated sympathetic activity and reduced parasympathetic activity.5,6) Accordingly, an unexpected increase in sympathetic activity can excessively elevate BP and/or heart rate (HR) during exercise, even at low or moderate intensity. 7) One previous study reported that hypertensive patients who had increased sympathetic activity during exercise developed LVH more rapidly compared to those without autonomic imbalance. 8)Skeletal muscles are known to accumulate metabolites such as lactic acid during exercise. 9) These metabolites stimulate the rostral ventrolateral medulla, which is the center of the sympathetic system, via metabolite-sensitive receptors in skeletal m...

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Influence of nifedipine coat-core and amlodipine on systemic arterial stiffness modulated by sympathetic and parasympathetic activity in hypertensive patients

Cited by 7 publications

References 35 publications

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

Early intervention of long-acting nifedipine GITS reduces brachial–ankle pulse wave velocity and improves arterial stiffness in Chinese patients with mild hypertension: a 24-week, single-arm, open-label, prospective study

Muscle Weakness Is Associated With an Increase of Left Ventricular Mass Through Excessive Blood Pressure Elevation During Exercise in Patients With Hypertension

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Influence of nifedipine coat-core and amlodipine on systemic arterial stiffness modulated by sympathetic and parasympathetic activity in hypertensive patients

Cited by 7 publications

References 35 publications

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

L/N-Type Calcium Channel Blocker Cilnidipine Added to Renin-Angiotensin Inhibition Improves Ambulatory Blood Pressure Profile and Suppresses Cardiac Hypertrophy in Hypertension with Chronic Kidney Disease

Early intervention of long-acting nifedipine GITS reduces brachial&ndash;ankle pulse wave velocity and improves arterial stiffness in Chinese patients with mild hypertension: a 24-week, single-arm, open-label, prospective study

Muscle Weakness Is Associated With an Increase of Left Ventricular Mass Through Excessive Blood Pressure Elevation During Exercise in Patients With Hypertension

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Early intervention of long-acting nifedipine GITS reduces brachial–ankle pulse wave velocity and improves arterial stiffness in Chinese patients with mild hypertension: a 24-week, single-arm, open-label, prospective study