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. Author manuscript; available in PMC: 2023 Mar 9.
Published in final edited form as: Microcirculation. 2021 Oct 21;28(8):e12733. doi: 10.1111/micc.12733

FIGURE 10.

FIGURE 10

KCa channels contribute to hyperpolarization of ECs more than SMCs in response to CGRP. (A) Representative recording of Vm from an EC within a MA endothelial tube demonstrates lack of hyperpolarization to CGRP in the presence of charybdotoxin (ChTx; 10−7 M) + apamin (AP; 3 × 10−7 M); note hyperpolarization to ACh (5 min) following washout, confirming EC viability. (B) Summary data for Vm responses to CGRP in SMCs from intact MAs (+EC) studied at 37°C under control conditions (from Figure 2) or during KCa channel inhibition. (C) Summary data for Vm responses to CGRP in ECs within endothelial tubes studied at 32°C in the presence or absence of KCa channel inhibitors. Values are means ± SEM for n = 5 per group. B = baseline Vm. W = washout in control PSS. #p < 0.05 vs. baseline (prior to application of CGRP) Vm in vessels treated with ChTx + AP. †p < 0.05 vs. control. *p < 0.05 EC vs. SMC Vm