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Thursday, December 27, 2018 12:53:23 PM
Here is a snippet of usefull info:
The problem with DHPs from a therapeutic perspective, however, is that they are not selective12. LTCCs are a heterogenous class of multi-subunit ion channels13,14 that can be divided into four classes based on the identity of their pore-forming alpha 1 subunit, CaV1.1-4. This pore-forming subunit governs key features of the channel, including gating and pharmacology. The predominant (~90%) LTCC in the brain has a CaV1.2 subunit; this channel also is abundant in a variety of peripheral organ systems, including the cardiovascular system and is effectively antagonized by DHPs, accounting for their therapeutic efficacy in hypertension15. However, the LTCC responsible for mitochondrial oxidant stress and increased vulnerability in SNc dopaminergic neurons is largely attributable to expression of LTCCs with a CaV1.3 subunit5,6. Among the DHPs, isradipine has the highest relative affinity for CaV1.3 LTCCs, but it is still CaV1.2 LTCC selective14. This diminishes the therapeutic potential of DHPs in PD, as cardiovascular side effects limit the dosing and antagonism of CaV1.3 LTCCs. As there are no selective CaV1.3 LTCC antagonists known, there is a real translational need to develop a new therapeutic agent.
The antagonistic effects of well-known LTCC antagonists16,17, like isradipine, verapamil and diltiazem (Fig. 1a), were investigated with
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