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Some studies suggest amlodipine increases heart rate in light conditions, while other studies do not directly address its effect on heart rate.
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Amlodipine, a long-acting calcium channel blocker, is widely used in the treatment of hypertension and angina pectoris. Its primary mechanism involves the relaxation of blood vessels, which helps to lower blood pressure. However, its effects on heart rate (HR) have been a subject of various studies, with mixed findings.
Several studies have investigated the influence of amlodipine on heart rate variability (HRV), a measure of the autonomic regulation of the heart. In hypertensive patients with stable angina pectoris, amlodipine did not significantly change HRV time domain parameters, indicating a stable heart rate over the treatment period. This suggests that amlodipine does not have a substantial impact on heart rate variability.
When compared to other calcium channel blockers like nifedipine, amlodipine showed a different profile. Amlodipine decreased plasma and urinary norepinephrine levels, which are markers of sympathetic nerve activity, during chronic treatment. This reduction in sympathetic activity was not observed with short-acting nifedipine, which actually increased these levels. This indicates that amlodipine may have a more stabilizing effect on heart rate compared to some other calcium channel blockers.
In a study assessing the hemodynamic effects of intravenous amlodipine in patients with stable angina, a slight increase in heart rate was observed shortly after administration. The heart rate increased from 75 to 80 beats per minute, which was statistically significant. This transient increase in heart rate could be attributed to the initial vasodilatory effect of the drug, which may trigger a reflex tachycardia.
Long-term studies have shown that amlodipine does not significantly alter heart rate. For instance, in a study involving patients with coronary artery disease, amlodipine reduced the frequency of ischemic episodes without significantly affecting heart rate. Similarly, in animal studies, amlodipine did not significantly affect heart rate during periods of induced ischemia.
A study on the circadian effects of amlodipine in rats found that the drug caused a dose-dependent increase in heart rate, which was more pronounced during the light phase of the day. This suggests that the time of administration may influence the heart rate response to amlodipine.
In summary, while amlodipine may cause a slight, transient increase in heart rate immediately after administration, it generally does not have a significant long-term impact on heart rate. Its effects on heart rate variability and sympathetic nerve activity suggest a stabilizing influence, making it a suitable option for patients requiring long-term management of hypertension and angina. The circadian phase-dependency observed in animal studies indicates that the timing of administration could be an important factor in its cardiovascular effects. Overall, amlodipine appears to be a safe and effective medication with minimal adverse effects on heart rate.
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