**4.2 T-type Ca2+ channels**

T-type Ca2+ channels are formed by pore-forming α1 subunits with similar topology as that of the LTCC α1c subunit, but with no known auxiliary subunits that modulate channel function [74]. TTCCs are activated at more hyperpolarized potentials and show similar conductance with Ca2+ or Ba2+ as charge carriers. Vascular smooth muscle cells express several TTCC α1 subunits, including CaV3.1 (α1G) and CaV3.2 (α1H) [9, 94–98]. Intriguingly, CaV3.1, which is found in murine vascular smooth muscle, seems to be replaced by CaV3.3 (α1I) in human cells [96], suggesting that expression of TTCC α1 subunits is species-dependent. TTCCs have been shown to contribute to vascular smooth muscle excitability in several vascular beds from different species [9, 98]. However, rigorous analysis revealed that different CaV3.X subunits may have very divergent physiological responses. For instance, whereas CaV3.1 (CaV3.3) mediates low-pressure-induced constriction, CaV3.2 contributes to the negative feedback regulation of vascular tone by stimulating the RyR/BKCa axis (**Figure 3**) [64, 95, 96]. TTCCs can also be regulated by signaling molecules. Indeed, the NO/PKG and AC/PKA axes both inhibit vascular TTCCs [99, 100], which may have key implications in vascular smooth muscle excitability. Whether these signaling molecules are organized and targeted by scaffold proteins such as AKAPs to areas near TTCCs to fine-tune their function is unclear and therefore the subject of future studies.
