This paper quantifies recent experimental results through a general physical description of the mechanisms that might control two fundamental cellular parameters, resting potential (E_m) and cell volume (V_c), thereby clarifying the complex relationships between them. It determined E_m directly from a charge difference (CD) equation involving total intracellular ionic charge and membrane capacitance (C_m). This avoided the equilibrium condition dE_m/dt = 0 required in determinations of E_m by previous work based on the Goldman-Hodgkin-Katz equation and its derivatives and thus permitted precise calculation of E_m even under non-equilibrium conditions. It could additionally accurately model the influence upon E_m of changes in C_m or V_c and of membrane transport processes such as the Na⁺-K⁺-ATPase and ion co-transport. Given a stable and adequate membrane Na⁺-K⁺-ATPase density (N), V_c and E_m both converged to unique steady-state values even from sharply divergent initial intracellular ionic concentrations. For any constant set of transmembrane ion permeabilities, this set point of V_c was then determined by the intracellular membrane-impermeant solute content (X^-_i) and its mean charge valency (z_X), while in contrast, the set point of E_m was determined solely by z_X. Independent changes in membrane Na⁺ (P_Na) or K⁺ permeabilities (P_K) or activation of cation-chloride co-transporters could perturb V_c and E_m but subsequent reversal of such changes permitted full recovery of both V_c and E_m to the original set points. Proportionate changes in P_Na, P_K and N, or changes in Cl^- permeability (P_Cl), instead conserved steady-state V_c and E_m but altered their rates of relaxation following any discrete perturbation. P_Cl additionally determined the relative effect of co-transporter activity on V_c and E_m, in direct agreement with recent experimental results. In contrast, changes in X^-_i produced by introduction of a finite permeability term to X^- (P_X) that did not alter z_X caused sustained changes in V_c that were independent of E_m and that persisted when P_X returned to zero. Where such fluxes also altered the effective z_X they additionally altered the steady state E_m. This offers a basis for the suggested roles of amino acid fluxes in long-term volume regulatory processes in a variety of excitable tissues.