Kir2 channels control the resting membrane voltage in many electrically excitable cells, and heritable mutations cause periodic paralysis and cardiac arrhythmia.
However, many electronically excitable cells and tissues in the human body including neurons and cardiac tissue exhibit Young's moduli between 1 and 10 kPa.
In addition to a fast activating and immediately inactivating sodium current, the inward current of many types of excitable cells also has a non-inactivating or slowly inactivating component: the persistent sodium current (INaP).
In addition to a fast activating and immediately inactivating inward sodium current, many types of excitable cells possess a noninactivating or slowly inactivating component: the persistent sodium current (INaP).
Receptor-mediated Ca2+ signaling in many non-excitable cells initially induces Ca2+ release from intracellular Ca2+ stores, followed by Ca2+ influx across the plasma membrane.
Like in many non-excitable cells, the store-operated capacitative calcium entry in ECs is the main mechanism responsible for the agonist-induced calcium entry [ 21, 22].
Indeed, the stimulation of many non-excitable cells by neurotransmitters or hormones causes the parallel activation of the cAMP and the phosphoinositide signaling pathways [ 1, 2].
However, inwardly-rectifying K+ currents have also been described in many non-excitable cells, including epithelium, endothelium and granulocytes [ 3- 5], where the setting of resting membrane potential may also influence stimulus-secretion coupling.
Plants have their own excitable cells, many of them in a region just behind the root tip.
