Mechanosensitive signalling in fish gill and other ion transporting epithelia

Epithelia involved in vectorial salt transport respond to apical and basolateral changes in osmotic activity by moderating the transmural solute transport rate simultaneously with underlying volume regulatory mechanisms involved in regulatory volume increase (RVI) and decrease (RVD). This review examines rapid osmotic responses in salt secreting epithelia of marine and euryhaline teleost fish, with inclusion of recent results from other ion transporting epithelia that also respond rapidly to osmotic shock. Mitochondrion-rich chloride secreting cells of marine teleost fish gills and skin, when exposed to hypertonic shock, activate NaCl secretion via phosphorylation of Na(+), K(+), 2Cl(-) cotransporter (NKCC1) in the basolateral membrane and activation of anion channels in the apical membrane. Conversely, NaCl secretion is inhibited when chloride secreting cells are swollen osmotically. Mammalian airway epithelial cells also possess NKCC1 basally and apical anion channels [Cystic Fibrosis Transmembrane conductance Regulator (CFTR)]; with hypotonic shock, this epithelium releases ATP and NaCl secretion is stimulated via purinergic receptors, while hypertonic shock inhibits Na(+) uptake. In the eye, the ciliary epithelium activates Cl(-) channels in response to hypotonic shock as RVD, an effect that modulates transepithelial fluid transport rates. In the renal A6 cell line, K(+) and Cl(-) effluxes activate during RVD and RVI Na(+) transepithelial absorption. A common theme in these systems is ATP release in hypotonic shock with subsequent RVD-effective mechanisms such as NKCC1 inhibition and K(+) and Cl(-) efflux, but there are different effects of osmotic changes on transepithelial transport, apparently depending on the role of the epithelial system.