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Updated: Aug 13, 2026

Isolation and Kv Channel Recordings in Murine Atrial and Ventricular Cardiomyocytes
Published on: March 12, 2013
[Ca channel blocker and heart failure]
Shintaro Kinugawa1, Hiroyuki Tsutsui
1Department of Cardiovascular Medicine, Hokkaido University Graduate School of Medicine.
Insights
Calcium channel blockers (CCBs) initially showed promise for heart failure (HF) but short-acting versions increased risks. Newer CCBs offer potential therapeutic benefits for chronic HF patients.
Area of Science:
- Cardiovascular Pharmacology
- Pharmacology of Calcium Channel Blockers
Context:
- Calcium channel blockers (CCBs) target L-type calcium channels in vascular smooth muscle, lowering blood pressure.
- Initial expectations suggested CCBs could treat heart failure (HF) due to vasodilation.
- Short-acting CCBs were found to increase morbidity and mortality in chronic HF patients.
Purpose:
- To evaluate the efficacy and safety of various calcium channel blockers in the context of heart failure treatment.
- To explore the mechanisms behind the adverse effects of short-acting CCBs in HF.
- To investigate the potential of newly developed CCBs for managing chronic heart failure.
Summary:
- Short-acting CCBs can exacerbate HF by increasing sympathetic activity and heart rate.
- Long-acting amlodipine demonstrated a neutral effect on HF morbidity and mortality.
- Novel CCBs targeting different calcium channels or sympathetic activity, and those with protective effects (nitric oxide, antioxidant), are promising for HF treatment.
Impact:
- Highlights the differential effects of CCB subclasses on heart failure outcomes.
- Identifies risks associated with certain CCBs in HF patients.
- Suggests new therapeutic avenues for managing chronic heart failure with advanced CCB formulations.
Abstract:
Ca channel blocker (CCB) inhibits the entry of calcium ion through L-type calcium channel in the vascular smooth muscle, and possesses the blood pressure lowering action. It was expected that CCB might be useful for the treatment of heart failure (HF) because of its vasodilating action. However, the prospective, randomized, double-blind, crossover studies have shown that the short-acting CCBs rather increase morbidity and mortality in patients with chronic HF during the long-term follow-up. It would be due to the fact that CCBs increase the sympathetic nerve activity and cause tachycardia in response to their acute vasodilating effects. Amlodipine, the long-acting CCB, has been shown to have a neutral effect on morbidity and mortality in patients with HF. Recently, new CCBs, which do not increase heart rate, have been developed. These drugs exert the inhibitory action for N- or T-type Ca channel or directly prevent sympathetic nerve activity. Furthermore, some CCBs may act protectively in HF by stimulating nitric oxide production and/or inhibiting oxidative stress. Newly developed CCBs promise to be useful for the treatment of chronic HF.
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