By H. Babaei
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Extra info for Antihypertensive Drugs
2011b). Thus, cilnidipine is expected to provide synergistic and effective therapeutic strategies when administered with angiotensin II receptor blockers. 3 Abbreviation of prolonged QT-interval The heart of canine chronic atrioventricular block model (cardiac sudden death model) is known to have a ventricular electrical remodeling, which mimics the pathophysiology of long QT syndrome (Sugiyama, 2008). Using this model, we explored a new pharmacological therapeutic strategy for prevention of cardiac sudden death (Fig.
Since cilnidipine directly inhibits the sympathetic neurotransmitter release by N-type Ca2+ channel-blocking property, the drug can be expected as 4th generation, providing an effective strategy for the treatment of cardiovascular diseases (Takahara, 2009). Recently, cilnidipine has been demonstrated to suppress renin-angiotensin-aldosterone system at anti-hypertensive doses in animal examinations, whereas other Ca2+ channel blockers usually activates such vasopressor system after acute or repeated administrations.
This may provide synergistic and effective therapeutic strategies during combined administration of cilnidipine and angiotensin II receptor blockers. The possible mechanisms to suppress reninangiotensin-aldosterone system appear to be clarified. In human adrenocortical cells, where N-type Ca2+ channels are recently found to act as a source of intracellular Ca2+ mobilization, cilnidipine as well as a specific N-type Ca2+ channel blocker ω-conotoxin effectively inhibits angiotensin II-induced aldosterone synthesis.