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

H. M. Prior, M. S. Yates and D. J. Beech

1. 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.

2. Single cells had a mean resting potential of -38 mV and were depolarized by 130 mM K⁺ but not by the Cl^- channel blocker 4,4'-diisothiocyanatostilbene-2,2'-disulphonic acid (DIDS).

3. Iberiotoxin did not affect the resting potential but inhibited spontaneous transient hyperpolarizations. Iberiotoxin or 1 mM 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.

4. A voltage-independent K⁺ current was inhibited by 0·1 mM barium (Ba²⁺) and unaffected by iberiotoxin, glibenclamide, apamin, 3,4-DAP and ouabain. In six out of ten cells, 1 mM Ba²⁺ depolarized the resting potential, while in the other cells the potential was resistant to all of the K⁺ channel blockers and ouabain. Ba²⁺ (0·1-1 mM) constricted the intact artery, but 10 µM Ba²⁺, 1 µM glibenclamide or 100 nM apamin had no effect.

5. The data suggest that resting potential is determined by background K⁺ channels, one type being Ba²⁺ sensitive and voltage independent, and another type being poorly defined due to its resistance to any inhibitor. Large conductance Ca²⁺-activated K⁺ (BK_Ca) and K_V channels do not determine the resting potential but have separate functions to underlie transient Ca²⁺-induced hyperpolarizations and to protect against depolarization past about -30 mV.

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