Reflex tachycardia from a calcium antagonist is a baroreflex response: vasodilation lowers pressure, baroreceptors fire less, and sympathetic outflow rises, releasing noradrenaline that speeds the heart. The release of noradrenaline at sympathetic terminals is gated by $N$-type voltage-gated calcium channels.
Cilnidipine is a dual $L/N$-type blocker. Its $L$-type action relaxes vascular smooth muscle to lower BP, while its $N$-type action at the sympathetic nerve ending suppresses the very noradrenaline release that would otherwise drive the reflex heart-rate rise:
$N\text{-type blockade} \Rightarrow \downarrow \text{noradrenaline release} \Rightarrow \text{no reflex tachycardia}$
T-type and R-type channels are not the sympathetic-terminal target responsible for this benefit.
\[\boxed{\text{Cilnidipine additionally blocks N-type Ca}^{2+}\text{ channels}}\]