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These studies suggest amlodipine can increase heart rate more pronouncedly in light conditions while generally reducing blood pressure and improving heart function.
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Amlodipine, a long-acting calcium channel blocker, is widely used in the treatment of hypertension and angina pectoris. Its effects on heart rate (HR) are of significant interest, particularly in understanding its impact on cardiovascular health and autonomic nervous system regulation.
Studies have shown that amlodipine does not significantly alter heart rate variability (HRV) time domain parameters in hypertensive patients with stable angina pectoris and isolated left ventricular diastolic dysfunction. However, it does reduce total power, very low frequency power, and low frequency power, indicating a reduction in sympathetic autonomic nervous system activity. This suggests that amlodipine may shift the autonomic balance towards increased vagal activity, which is beneficial for heart rate control.
The timing of amlodipine administration can influence its effects on heart rate. A study comparing morning and evening dosing found that morning administration had a more favorable impact on circadian blood pressure and heart rate patterns. Specifically, morning dosing resulted in a greater nocturnal fall in blood pressure and a more stable heart rate throughout the day. This indicates that the timing of amlodipine administration can be optimized to enhance its cardiovascular benefits.
Amlodipine has been shown to increase heart rate slightly when administered intravenously. In a study involving subjects with stable angina pectoris, heart rate increased from 75 to 80 beats per minute following amlodipine administration, accompanied by a decrease in systemic vascular resistance and mean arterial pressure. These hemodynamic changes highlight amlodipine's vasodilatory effects, which can influence heart rate.
When compared to nifedipine, another calcium channel blocker, amlodipine has a distinct effect on sympathetic nerve activity. Amlodipine administration did not induce an increase in sympathetic nerve activity in essential hypertensive patients during chronic treatment, unlike nifedipine, which increased plasma and urinary norepinephrine levels. This suggests that amlodipine may have a more stable effect on heart rate by not triggering reflex sympathetic activation.
In animal studies, amlodipine has shown a dose-dependent increase in heart rate, with more pronounced effects during the light span compared to the dark span. This circadian phase-dependency indicates that the cardiovascular effects of amlodipine, including its impact on heart rate, can vary based on the time of administration.
Amlodipine's effects on heart rate are multifaceted, involving changes in heart rate variability, circadian rhythms, and sympathetic nerve activity. While it generally stabilizes heart rate by reducing sympathetic activity and enhancing vagal tone, the timing of administration and comparison with other calcium channel blockers like nifedipine reveal nuanced differences in its cardiovascular impact. Understanding these effects can help optimize amlodipine use for better cardiovascular outcomes.
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