= Solution
Write the instantaneous <electrical conductance> as $g_K(t)=\bar g_K n(t)^4$. Here $\bar g_K$ is the maximal <electrical conductance> of the recorded membrane, $n$ is the activation variable, $V_m$ is inside-minus-outside <membrane potential>, and $V_K$ is the <potassium> <Nernst equilibrium potential>. The factor $V_m-V_K$ is the electrochemical driving <voltage>; positive $I_K$ conventionally denotes outward positive charge. For an <electric current> density, $\bar g_K$ must instead be an <electrical conductance> per area.
In the <Hodgkin-Huxley model>, four equivalent independent activation gates must all be permissive, each with <probability> $n$, so their joint opening <probability> is $n^4$. At fixed <voltage> each gate obeys
$$
\dot n=\alpha_n(V_m)(1-n)-\beta_n(V_m)n,\qquad
n_\infty=\frac{\alpha_n}{\alpha_n+\beta_n},\quad
\tau_n=\frac1{\alpha_n+\beta_n}.
$$
The model assumes approximately Ohmic open-channel conduction, a well-defined population-average <electrical conductance>, and an almost constant <potassium> <reversal potential> during a brief recording. Four phenomenological gates should not be mistaken for a proof of four physically independent molecular transitions. The simple delayed-rectifier description also omits <ion-channel inactivation>.
Reducing the available <electrical conductance> can weaken <repolarization>, broaden an <action potential> and alter repetitive firing. Depending on channel class and tissue, excess excitability or impaired recovery can follow; persistent depolarization can also reduce <voltage-gated sodium channel> availability. Cardiac potassium-current reductions can prolong the <action potential> and contribute to <Long QT syndrome>. These are conditional physiological consequences, not a claim that every potassium-current reduction has the same clinical effect.
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