Potassium channel selectivity in mouse pancreatic B cells

Abstract

High-resistance microelectrodes were used to measure membrane potential changes in response to increased extracellular K+ concentration ([K+]o; or a test cation X+ such as Li+, Rb+, Cs+, NH+4) in B cells from mouse islets of Langerhans. In the absence of glucose, a sudden increase in [K+]o (or [X+]o), keeping the sum [Na+]o + [K+]o constant (or [Na+]o + [K+]o + [X+]o), induced a rapid depolarization of the membrane. The membrane potential changes were essentially unchanged in the presence of 20 mM tetraethylammonium (TEA). The Goldman-Hodgkin-Katz equation was fitted to the experimental relationship between membrane potential and [K+]o (or [X+]o), and permeability (P) ratios were estimated. In the absence of TEA, P Na/PK was estimated to be approximately 0.046. In the presence of TEA the following ratios were estimated: P Rb/PK = 0.74, P Cs/PK = 0.62, and P NH4/PK = 0.36. From these ratios the following sequence of permeabilities was obtained, PK greater than P Rb greater than P Cs greater than P NH4 greater than P Na. It is proposed that this sequence reflects the selectivity of the intracellular [Ca2+]-activated K+ channel of the pancreatic B cell.

Permeability characteristics of monovalent cations in atrial myocytes of the rat heart

“…However, significant permeability (P) to Cs¤ of voltagedependent K¤ channels was also reported (PCsÏPK = 0·16, Hadley & Hume, 1990; PCsÏPK = 0·62, Rosario & Rojas, 1986; PCsÏPK = 0·11, Gay & Stanfield, 1978). In the present study, we showed a substantial degree of Cs¤ permeability through the IKr channel.…”

Characterization of potassium channels in pancreatic β cells from ob/ob mice

“…The pancreatic islets from the ob/ob strain of mice (Norwich colony, UK) have been shown to display subtle abnormalities in the membrane potential fluctuations stimulated by glucose and to be relatively insensitive to sulfonylureas [5,6]. We found that the pancreatic ~ cells from the same ob/ob strain of mice (Jackson Laboratory colony) have the 3 kinds of potassium channels characterized in normal rats, mice, humans and islet-derived cell lines.…”

“…Defects in the potassium permeability of some diabetic mouse models have been reported [3]. Membrane potential measurements in pancreatic islets from homozygous db/db (diabetic) and ob/ob (obese) mice show abnormalities in the response to glucose consistent with a defective potassium conductance [4][5][6].…”

Modulation of gating of a metabolically regulated, ATP-dependent K+ channel by intracellular pH in B cells of the pancreatic islet

“…This suggests a steady-state cell depolarization. The K+(ATP) channel may be somewhat permeable to NH4C1 in that, at rest, the B-cell membrane is estimated to be roughly 1/3 as permeable to NH2 as to K + (Rosario & Rojas, 1986a). Assuming (i) that NH~-acts as a permeant blocker of the K+(ATP) channel from the cytoplasmic surface of the membrane, as it does with the K+(Ca 2+) channel (see Tabcharani & Misler, 1989), and (ii) the K+(ATP) channel of the B cell, like the K+(Ca 2+) channel, behaves like a multi-ion channel where mutual repulsion between cations augments their traversal of the membrane, two predictions seem reasonable.…”