Cell-attached recordings revealed K+ channel activity in basolateral membranes of guinea pig distal colonic crypts. Inwardly rectified currents were apparent with a pipette solution containing 140 mM K+. Single-channel conductance (γ) was 9 pS at the resting membrane potential. Another inward rectifier with γ of 19 pS was observed occasionally. At a holding potential of −80 mV, γ was 21 and 41 pS, respectively. Identity as K+ channels was confirmed after patch excision by changing the bath ion composition. From reversal potentials, relative permeability of Na+ over K+ (P Na/P K) was 0.02 ± 0.02, withP Rb/P K = 1.1 andP Cl/P K < 0.03. Spontaneous open probability (P o) of the 9-pS inward rectifier (gpKir) was voltage independent in cell-attached patches. Both a low (P o = 0.09 ± 0.01) and a moderate (P o = 0.41 ± 0.01) activity mode were observed. Excision moved gpKirto the medium activity mode; P o ofgpKir was independent of bath Ca2+activity and bath acidification. Addition of Cl− and K+ secretagogues altered P o ofgpKir. Forskolin or carbachol (10 μM) activated the small-conductance gpKir in quiescent patches and increased P o in low-activity patches. K+ secretagogues, either epinephrine (5 μM) or prostaglandin E2 (100 nM), decreasedP o of gpKir in active patches. This gpKir may be involved in electrogenic secretion of Cl− and K+across the colonic epithelium, which requires a large basolateral membrane K+conductance during maximal Cl− secretion and, presumably, a lower K+conductance during primary electrogenic K+ secretion.