Question

Cilnidipine is unique among dihydropyridine calcium channel blockers in not causing reflex tachycardia. This is because, in addition to L-type channels, it also blocks which type of voltage-gated calcium channel located on sympathetic nerve endings?

• A. T-type
• B. R-type
• C. N-type
• D. L-type

Hint:

N-type channels on sympathetic terminals control noradrenaline release.

Answer 1

The Correct Option is C

Step 1: Recall the basis of reflex tachycardia with DHPs.
Conventional dihydropyridines (e.g., amlodipine, nifedipine) block L-type calcium channels, causing arteriolar vasodilation and a fall in blood pressure. The baroreceptor reflex then activates the sympathetic system, releasing noradrenaline and producing reflex tachycardia.

Step 2: Identify Cilnidipine's extra target.
Cilnidipine is an L/N-type calcium channel blocker. The N-type channels sit on sympathetic (postganglionic) nerve terminals and control calcium-dependent noradrenaline release.

Step 3: Link mechanism to the clinical effect.
By blocking N-type channels, Cilnidipine reduces sympathetic noradrenaline release. So even when L-type blockade lowers BP, the compensatory sympathetic surge is blunted - hence no reflex tachycardia.

Step 4: Eliminate the others.
T-type channels are targeted by mibefradil/efonidipine (different profile); R-type are not the relevant sympathetic target here; L-type blockade alone is what causes the reflex problem. The answer is N-type.

Key fact: Cilnidipine blocks N-type Ca channels on sympathetic nerve endings, preventing reflex tachycardia.