FUNCTIONS OF LARGE-CONDUCTANCE CA2-ACTIVATED (BKCA), DELAYED RECTIFIER (K-V) AND BACKGROUND K+ CHANNELS IN THE CONTROL OF MEMBRANE-POTENTIAL IN RABBIT RENAL ARCUATE ARTERY()

1. The types of K+ channel which determine the membrane potential of a rcuate artery smooth muscle cells were investigated by patch-clamp rec ording from isolated cells and lumenal diameter measurements from inta ct pressurized renal arcuate arteries. 2. Single cells had a mean rest ing potential of -38 mV and were depolarized by 130 mM K+ but not by t he Cl- channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS). 3. Iberiotoxin did not affect the resting potential but i nhibited spontaneous transient hyperpolarizations. Iberiotoxin or 1 mM tetraethlylammonium (TEA(+)) constricted intact arteries. 3,4-Diamino pyridine (3,4-DAP)-sensitive delayed rectifier K+ (K-v) channel curren t was elicited by depolarization but 3,4-DAP did not affect the restin g potential or induce constriction in the intact artery. 4. A voltage- independent K+ current was inhibited by greater than or equal to 0.1 m M barium (Ba2+) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain. In six out of ten cells, 1 mM Ba2+ depolarized th e resting potential, while in the other cells the potential was resist ant to all of the K+ channel blockers and ouabain. Ba2+ (0.1-1 mM) con stricted the intact artery but 10 mu M Ba2+, 1 mu M glibenclamide or 1 00 nM apamin had no effect. 5. The data suggest that resting potential is determined by background K+ channels, one type being Ba2+ sensitiv e and voltage independent, and another type being poorly defined due t o its resistance to any inhibitor. Large conductance Ca2+-activated K (BKCa) and K-V, channels do not determine the resting potential but h ave separate functions to underlie transient Ca2+-induced hyperpolariz ations and to protect against depolarization past about -30 mV.