4) were fitted to simulated conduction profiles in the SMC layer. 3) and a sum of two exponentials with reflection (Eq. Also, it illustrates the necessity of using and developing models that handle the nonlinearity of ion channels. This may have implications in relation to explaining why different agonists have different conduction properties. As ion channels have time-dependent activation and inactivation, the conduction profile changes considerably during this dynamic period with an initially longer spread of current. In contrast, using the model it is possible to probe how conduction behaves before steady state is achieved. Determination of λ using cable theory assumes steady-state conditions. Hence, λ should be interpreted as a descriptive measure and not in light of cable theory. However, the phenomenological use of a length-constant from a single exponential function is a good measure of conduction length. We find that several important cable theory assumptions are violated when applied to small blood vessels. We have employed a morphologically and electrophysiologically detailed mathematical model of a rat mesenteric arteriole to investigate if the assumptions hold and whether λ adequately describes simulated conduction profiles. However, the applicability of cable theory to blood vessels depends on assumptions that are not necessarily fulfilled in small arteries and arterioles. The decay is typically quantified using the steady-state length-constant, λ, derived from cable theory. Conduction processes in the vasculature have traditionally been described using cable theory, i.e., locally induced signals decaying passively along the arteriolar wall.
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