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These studies suggest that amlodipine can increase heart rate more pronouncedly in light conditions while generally reducing blood pressure and not significantly affecting heart rate in other contexts.
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Amlodipine, a calcium channel blocker, is widely used in the treatment of hypertension and angina pectoris. Its effects on heart rate (HR) are of particular interest due to its role in cardiovascular therapy. This article synthesizes findings from multiple studies to provide a comprehensive overview of how amlodipine influences heart rate.
Several studies have documented that amlodipine administration can lead to a modest increase in heart rate. For instance, in a study involving subjects with stable angina pectoris, intravenous administration of 10 mg amlodipine resulted in an increase in heart rate from 75 ± 12 beats/min to 80 ± 15 beats/min, which was statistically significant (p < 0.05). This increase was observed for at least 15 minutes post-administration.
The timing of amlodipine administration can influence its effects on heart rate. A study comparing morning and evening dosing of amlodipine in patients with mild-to-moderate essential hypertension found that the increase in heart rate was more pronounced when the drug was administered in the morning compared to the evening. This suggests a circadian phase-dependency in the cardiovascular effects of amlodipine.
Amlodipine has been shown to affect heart rate variability (HRV), which is a measure of autonomic nervous system activity. In hypertensive patients with stable angina pectoris, amlodipine did not significantly change HRV time domain parameters but did reduce the low-high frequency ratio, indicating a shift towards increased vagal activity. This shift suggests a reduction in sympathetic nervous system activity, which can be beneficial in managing cardiovascular conditions.
Further supporting the reduction in sympathetic activity, another study found that chronic administration of amlodipine decreased plasma and urinary norepinephrine levels, a marker of sympathetic nerve activity. This reduction was not observed with short-acting nifedipine, highlighting a unique benefit of amlodipine in reducing sympathetic activation.
In animal models, the effects of amlodipine on heart rate have also been studied. In male Wistar rats, amlodipine administration led to a dose-dependent increase in heart rate, with more pronounced effects observed during the light phase of the circadian cycle. This aligns with findings in human studies, suggesting that the time of administration can influence the drug's impact on heart rate.
Amlodipine's ability to modulate heart rate and reduce sympathetic activity may contribute to its cardioprotective effects. For example, in patients with coronary artery disease, amlodipine significantly reduced both symptomatic and asymptomatic ischemic events over 24 hours. This reduction in ischemic events, coupled with a favorable autonomic profile, underscores the therapeutic potential of amlodipine in cardiovascular disease management.
Despite its effects on heart rate, amlodipine is generally well-tolerated. It does not cause significant reflex tachycardia or cardiac conduction disturbances, making it a safe option for long-term use in patients with hypertension and angina pectoris.
Amlodipine has a modest but significant effect on increasing heart rate, influenced by the timing of administration and circadian rhythms. It also positively affects heart rate variability by reducing sympathetic nerve activity, which can be beneficial in managing cardiovascular conditions. These findings highlight the importance of considering both the timing and chronic effects of amlodipine in clinical practice to optimize cardiovascular outcomes.
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