Functions of large conductance Ca2+-activated (BKCa), delayed rectifier (KV) and background K+ channels in the control of membrane potential in rabbit renal arcuate artery

The types of K + channel which determine the membrane potential of arcuate artery smooth muscle cells were investigated by patch-clamp recording from isolated cells and lumenal diameter measurements from intact pressurized renal arcuate arteries. Single cells had a mean resting potential of -38 mV and were depolarized by 130 m m K + but not by the Cl − channel blocker 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS). Iberiotoxin did not affect the resting potential but inhibited spontaneous transient hyperpolarizations. Iberiotoxin or 1 m m tetraethylammonium (TEA + ) constricted intact arteries. 3,4-Diaminopyridine (3,4-DAP)-sensitive delayed rectifier K + (K V ) channel current was elicited by depolarization but 3,4-DAP did not affect the resting potential or induce constriction in the intact artery. A voltage-independent K + current was inhibited by ≥ 0·1 m m barium (Ba 2+ ) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain. In six out of ten cells, 1 m m Ba 2+ depolarized the resting potential, while in the other cells the potential was resistant to all of the K + channel blockers and ouabain. Ba 2+ (0·1-1 m m ) constricted the intact artery, but 10 μM Ba 2+ , 1 μM glibenclamide or 100 n m apamin had no effect. The data suggest that resting potential is determined by background K + channels, one type being Ba 2+ sensitive and voltage independent, and another type being poorly defined due to its resistance to any inhibitor. Large conductance Ca 2+ -activated K + (BK Ca ) and K V channels do not determine the resting potential but have separate functions to underlie transient Ca 2+ -induced hyperpolarizations and to protect against depolarization past about -30 mV.