A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle.

The function of the smooth muscle cells lining the walls of mammalian systemic arteries and arterioles is to regulate the diameter of the vessels to control blood flow and blood pressure. Here, we describe an in silico model, which we call the 'Hernandez-Hernandez model', of electrical and Ca signaling in arterial myocytes based on new experimental data indicating sex-specific differences in male and female arterial myocytes from murine resistance arteries. The model suggests the fundamental ionic mechanisms underlying membrane potential and intracellular Ca signaling during the development of myogenic tone in arterial blood vessels.

The formation of K2.1 macro-clusters is required for sex-specific differences in L-type Ca1.2 clustering and function in arterial myocytes.

In arterial myocytes, the canonical function of voltage-gated Ca1.2 and K2.1 channels is to induce myocyte contraction and relaxation through their responses to membrane depolarization, respectively.

The formation of K 2.1 macro-clusters is required for sex-specific differences in L-type Ca 1.2 clustering and function in arterial myocytes.

In arterial myocytes, the canonical function of voltage-gated Ca 1.2 and K 2.1 channels is to induce myocyte contraction and relaxation through their responses to membrane depolarization, respectively.

A computational model predicts sex-specific responses to calcium channel blockers in mammalian mesenteric vascular smooth muscle.

The function of the smooth muscle cells lining the walls of mammalian systemic arteries and arterioles is to regulate the diameter of the vessels to control blood flow and blood pressure. Here, we describe an model, which we call the "Hernandez-Hernandez model", of electrical and signaling in arterial myocytes based on new experimental data indicating sex-specific differences in male and female arterial myocytes from murine resistance arteries. The model suggests the fundamental ionic mechanisms underlying membrane potential and intracellular signaling during the development of myogenic tone in arterial blood vessels.

A stochastic model of ion channel cluster formation in the plasma membrane.

Ion channels are often found arranged into dense clusters in the plasma membranes of excitable cells, but the mechanisms underlying the formation and maintenance of these functional aggregates are unknown. Here, we tested the hypothesis that channel clustering is the consequence of a stochastic self-assembly process and propose a model by which channel clusters are formed and regulated in size. Our hypothesis is based on statistical analyses of the size distributions of the channel clusters we measured in neurons, ventricular myocytes, arterial smooth muscle, and heterologous cells, which in all cases were described by exponential functions, indicative of a Poisson process (i.

Nonlinear signaling on biological networks: The role of stochasticity and spectral clustering.

Signal transduction within biological cells is governed by networks of interacting proteins. Communication between these proteins is mediated by signaling molecules which bind to receptors and induce stochastic transitions between different conformational states. Signaling is typically a cooperative process which requires the occurrence of multiple binding events so that reaction rates have a nonlinear dependence on the amount of signaling molecule.

Publisher's Note: Role of connectivity and fluctuations in the nucleation of calcium waves in cardiac cells [Phys. Rev. E 92, 052715 (2015)].

This corrects the article DOI: 10.1103/PhysRevE.92.

Role of connectivity and fluctuations in the nucleation of calcium waves in cardiac cells.

Spontaneous calcium release (SCR) occurs when ion channel fluctuations lead to the nucleation of calcium waves in cardiac cells. This phenomenon is important since it has been implicated as a cause of various cardiac arrhythmias. However, to date, it is not understood what determines the timing and location of spontaneous calcium waves within cells.