T‐type voltage‐gated Ca(2+) channels do not contribute to the negative feedback regulation of myogenic tone in murine superior epigastric arteries

T‐type voltage‐gated Ca(2+) channels (CaV3.2 VGCC) have been hypothesized to control spontaneous transient outward currents (STOCs) through large‐conductance Ca(2+)‐activated K(+) channels (BK(Ca)), 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 μmol/L) STOCs at −30 mV, or cannulated and studied by pressure myography (80 cm H(2)O, 37°C). The CaV3.2 blocker Ni(2+) (30 μmol/L) had no effect on STOC amplitude (20.1 ± 1.7 pA vs. 20.6 ± 1.7 pA; n = 12, P = 0.6), but increased STOC frequency (0.79 ± 0.15 Hz vs. 1.21 ± 0.22 Hz; n = 12, P = 0.02). Although Ni(2+) produced concentration‐dependent constriction of isolated, pressurized SEAs (logEC(50) = −5.8 ± 0.09; E (max) = 72 ± 5% constriction), block of BK(Ca) with PAX had no effect on vasoconstriction induced by 30 μmol/L Ni(2+) (in the absence of PAX = 66 ± 4% constriction vs. in the presence of 1 μmol/L PAX = 65 ± 4% constriction; n = 7, P = 0.06). In contrast to Ni(2+), the nonselective T‐type blocker, mibefradil, produced only vasodilation (logEC(50 )= −6.9 ± 0.2; E (max) = 74 ± 8% dilation), whereas the putative T‐type blocker, ML218, had no significant effect on myogenic tone between 10 nmol/L and 10 μmol/L (n = 6–7, P = 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(2+) may constrict SEAs by means other than block of CaV3.2 VGCC.