Yang, Yan;
Ella, Srikanth R;
Murphy, Timothy V;
Grayson, T Hilton;
Hwang, Yun T;
Haddock, Rebecca;
Peichun, Gui;
Andrew, Braun P;
Korthuis, Ronald J;
Davis, Michael J;
Hill, Michael A
Relative lack of β1‐subunit‐mediated regulation of BKCa in cremaster arteriolar smooth muscle
Beschreibung:
<jats:sec><jats:label /><jats:p>The relationships between membrane potential (Em) and myogenic tone in skeletal muscle and cerebral arteries suggest differences in the role of BK<jats:sub>Ca</jats:sub>. To test this idea, whole cell K<jats:sup>+</jats:sup> currents were measured by patch clamp. At 5 μM Ca<jats:sup>2+</jats:sup>, 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<jats:sup>+</jats:sup> current to be due to BK<jats:sub>Ca</jats:sub>. 17β‐Estradiol, reported to act via the BK<jats:sub>Ca</jats:sub> β‐subunit, caused greater enhancement of K<jats:sup>+</jats:sup> current in cerebral SMC compared to those of cremaster. The α subunit‐selective BK<jats:sub>Ca</jats:sub> 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 Ca<jats:sup>2+</jats:sup> sparks (0/76 cells) relative to cerebral SMC (76/105 cells). Measurements of mRNA and protein indicated a higher ratio of BK<jats:sub>Ca</jats:sub> β:α‐subunit expression in cerebral SMC. The data suggest that decreased activity of BK<jats:sub>Ca</jats:sub> in cremaster SMC is due in part to a relative lack β‐subunit regulation.</jats:p></jats:sec>