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The exposure of brown adipocytes to extracellular ATP leads to exocytosis of intracellular membranes and increases the purinergic receptor mediated membrane trafficking. There is also a purinergic stimulated increase in the cell surface due to adipocyte vesicle-mediated secretion. The ATP exposure also increases the total cell membrane capacitance and the cytosolic calcium (Ca) levels. Adrenergic activation mobilizes calcium without influencing the amount of membrane trafficking. This indicates that the increase in Ca content is not solely responsible for the ATP-induced cellular responses.

The adrenergic depolarization of conductance in brown adipocytes is due to an increase in the intracellular calcium which stimulates a chloride-sensitive conductance. This conductance is different from the volume-sensitive chloride conductance of the cell. Cytoplasmic factors and intracellular calcium affect this chloride conductance. Cells cultured for short periods show depolarization of conductance more than those cultured for longer periods.

The most common channel observed in primary human peripheral T lymphocytes was voltage-gated and inactivating. This potassium channel comprise a majority of the outward current in lymphocytes. Another channel less frequently observed was transient and has a unitary conductance of nearly 10 pS. This channel is voltage-independent, lacks inactivation and has distinct kinetic parameters.