Figure 4.
Gap junctions facilitate the contribution of KCa2.3-channels to EDHF-hyperpolarization in rat mesenteric artery. A, Original traces demonstrating ACh-mediated concentration-dependent increases in smooth muscle cell membrane potential from the resting membrane potential (dashed lines). Carbenoxolone (100 μmol/L) did not alter the resting membrane potential, but reduced the hyperpolarization to ACh. B, Summarized data showing the average change in membrane potential (Δ Em) to cumulative increases in [ACh] to evoke EDHF-hyperpolarization in arteries from resting membrane potential (left, n=6-11). In the presence of PE (right panels), carbenoxolone (100 μmol/L) depressed EDHF hyperpolarization (n=5-9) but not relaxation to ACh (n=8-14). The EDHF-mediated relaxation was reduced by the addition of apamin (50 nmol/L, n=9-13), and almost abolished by TRAM-34 (1 μmol/L, n=5-12) or ouabain (100 μmol/L, n=3-9), each applied when carbenoxolone was present. Asterisk indicates significant difference relative to control (P<0.05).