Relative lack of β1‐subunit‐mediated regulation of BKCa in cremaster arteriolar smooth muscle

The relationships between membrane potential (Em) and myogenic tone in skeletal muscle and cerebral arteries suggest differences in the role of BKCa. To test this idea, whole cell K+ currents were measured by patch clamp. At 5 μM Ca2+, cremaster smooth muscle cells (SMC) showed lower current density compared to cerebral SMC (34.5±1.9 vs 45.5±1.7 pA pF‐1 at +70mV; p < 0.05). The selective inhibitor, iberiotoxin (0.1 μM), revealed the differences in K+ current to be due to BKCa. 17β‐Estradiol, reported to act via the BKCa β‐subunit, caused greater enhancement of K+ current in cerebral SMC compared to those of cremaster. The α subunit‐selective BKCa opener, NS1619, exerted similar effects in both types of SMC. Spontaneously transient outward currents (STOCs) were more evident and occurred at more negative Em in cerebral SMC. Also consistent with decreased STOC activity in cremaster SMC was an absence of Ca2+ sparks (0/76 cells) relative to cerebral SMC (76/105 cells). Measurements of mRNA and protein indicated a higher ratio of BKCa β:α‐subunit expression in cerebral SMC. The data suggest that decreased activity of BKCa in cremaster SMC is due in part to a relative lack β‐subunit regulation.