ABSTRACT
In most cells, the plasma membrane at rest is more permeable to K + than to Na +, Cl-and Ca2 +; therefore, K channels determine the resting membrane potential and, hence, the excitability of the cell. (A notable exception from this rule is skeletal muscle where the resting membrane potential is essentially governed by Clchannels (Hille, 1992)). The opening of K channels shifts the membrane potential towards the K+ equilibrium potential which is around -90 mV. For smooth muscle, which generally has a resting membrane potential of "'-60 mV, this means that opening of K channels hyperpolarizes the tissue; however, the value of -90 mV will only be reached asymptotically as the permeability to K + becomes absolutely dominating over that of the other ions (Hille, 1992). In excitable cells endowed with depolarization-activated Ca channels (voltage-gated Ca channels, VOCs ), hyperpolarization will prevent such channels from opening and, hence, Ca2 + entry via this pathway. In cells devoid of VOCs, e.g. endothelial cells, leukocytes and others, hyperpolarization will, by increasing the driving force for Ca2 + entry into the cell, promote Ca2+ influx via pathways which are active at such (hyperpolarized) membrane potentials.
