Expression and functional role of L‐type and T‐type calcium channels in conducted calcium responses to local KCl application in rat mesenteric terminal arterioles

Intracellular Ca 2+ signals underlying conducted vasoconstriction in rat mesenteric terminal arterioles were investigated using Ca 2+ imaging and micro‐ejection of isotonic KCl solution. We investigated the role of gap junctions and L‐, T‐type voltage‐dependent Ca 2+ channels (VDCCs) for conduction of Ca 2+ responses along the arteriolar wall. In 83 arterioles (ID = 25 ± 1 μm), local (0 μm) application of KCl lead to local Ca 2+ responses (from 89 nM to 316 nM) and conducted (500 μm) Ca 2+ responses (from 112 nM to 177 nM). Conducted Ca 2+ responses, only, were inhibited by gap junction uncouplers carbenoxolone and palmitoleic acid, but not by tetrodotoxin or low‐Na + PSS (n = 4–8). Bath application of the L‐type blocker nifedipine (0.1–10 μM) or the T‐type blockers mibefradil; NNC 55–0396 (both 0.1–10 μM); R(−)‐efonidipine (1–33 μM) blocked local and conducted Ca 2+ responses (n = 5). Localized block of Ca 2+ entry by micro‐pipette delivery of nifedipine or NNC 55–0396 (10 μM) had no effect on the conduction of Ca 2+ responses through the affected arteriolar segments (n = 4–5). Using immunocytochemistry and/or RT‐PCR, we detected expression of Ca V 1.2, Ca V 3.1 and Ca V 3.2 VDCCs in terminal arterioles. Our results suggest that L‐type and T‐type VDCCs both mediate Ca 2+ entry in VSMC during conducted vasoconstriction in rat mesenteric terminal arterioles. However, VDCCs are not crucially involved in the conduction mechanism.