T-type voltage-gated Ca channels do not contribute to the negative feedback regulation of myogenic tone in murine superior epigastric arteries.

T-type voltage-gated Ca channels (CaV3.2 VGCC) have been hypothesized to control spontaneous transient outward currents (STOCs) through large-conductance Ca-activated K channels (BK), and contribute to the negative-feedback regulation of myogenic tone. We tested this hypothesis in superior epigastric arteries (SEAs) isolated from male C57BL/6 mice. SEAs were isolated and enzymatically dissociated to obtain single smooth muscle cells (SMCs) for whole-cell recording of paxilline-sensitive (PAX, 1 mol/L) STOCs at -30 mV, or cannulated and studied by pressure myography (80 cm HO, 37°C). The CaV3.2 blocker Ni (30 mol/L) had no effect on STOC amplitude (20.1 ± 1.7 pA vs. 20.6 ± 1.7 pA;  = 12,  = 0.6), but increased STOC frequency (0.79 ± 0.15 Hz vs. 1.21 ± 0.22 Hz;  = 12,  = 0.02). Although Ni produced concentration-dependent constriction of isolated, pressurized SEAs (logEC = -5.8 ± 0.09;  = 72 ± 5% constriction), block of BK with PAX had no effect on vasoconstriction induced by 30 mol/L Ni (in the absence of PAX = 66 ± 4% constriction vs. in the presence of 1 mol/L PAX = 65 ± 4% constriction;  = 7,  = 0.06). In contrast to Ni, the nonselective T-type blocker, mibefradil, produced only vasodilation (logEC= -6.9 ± 0.2;  = 74 ± 8% dilation), whereas the putative T-type blocker, ML218, had no significant effect on myogenic tone between 10 nmol/L and 10 mol/L ( = 6-7,  = 0.59). Our data do not support a role for CaV3.2 VGCC in the negative-feedback regulation of myogenic tone in murine SEAs and suggest that Ni may constrict SEAs by means other than block of CaV3.2 VGCC.