Abstract
We review studies on regulatory volume decrease (RVD) and regulatory
volume increase (RVI) of major ion and water transporting vertebrate epithelia. The rate of RVD and RVI is faster in cells of high osmotic permeability like amphibian gallbladder and mammalian proximal tubule as compared to amphibian skin and mammalian cortical collecting tubule of low and intermediate osmotic permeability. Crosstalk between entrance and exit mechanisms interferes with volume regulation both at aniso-osmotic and iso-osmotic volume perturbations. It has been proposed that cell volume regulation is an intrinsic function of iso-osmotic fluid transport that depends on Na+ recirculation. The causative relationship is discussed for a fluid-absorbing and a fluid-secreting epithelium of which the Na+ recirculation mechanisms have been identified.
A large number of transporters and ion channels involved in cell volume regulation are cloned. The volume-regulated anion channel (VRAC) exhibiting specific electrophysiological characteristics seems exclusive to serve cell volume regulation. This is contrary to K+ channels as well as cotransporters and exchange mechanisms that may serve both transepithelial transport and cell volume regulation. In the same cell, these functions may be maintained by different ion pathways that are separately regulated. RVD is often preceded by increase in cytosolic free Ca2+, probably via influx through TRP channels, but Ca2+ release from intracellular stores has also been observed. Cell
volume regulation is associated with specific ATP release mechanisms and involves tyrosine kinases, mitogen-activated protein kinases, WNKs and Ste20-related kinases that are modulated by osmotic stress and cell volume perturbations.
volume increase (RVI) of major ion and water transporting vertebrate epithelia. The rate of RVD and RVI is faster in cells of high osmotic permeability like amphibian gallbladder and mammalian proximal tubule as compared to amphibian skin and mammalian cortical collecting tubule of low and intermediate osmotic permeability. Crosstalk between entrance and exit mechanisms interferes with volume regulation both at aniso-osmotic and iso-osmotic volume perturbations. It has been proposed that cell volume regulation is an intrinsic function of iso-osmotic fluid transport that depends on Na+ recirculation. The causative relationship is discussed for a fluid-absorbing and a fluid-secreting epithelium of which the Na+ recirculation mechanisms have been identified.
A large number of transporters and ion channels involved in cell volume regulation are cloned. The volume-regulated anion channel (VRAC) exhibiting specific electrophysiological characteristics seems exclusive to serve cell volume regulation. This is contrary to K+ channels as well as cotransporters and exchange mechanisms that may serve both transepithelial transport and cell volume regulation. In the same cell, these functions may be maintained by different ion pathways that are separately regulated. RVD is often preceded by increase in cytosolic free Ca2+, probably via influx through TRP channels, but Ca2+ release from intracellular stores has also been observed. Cell
volume regulation is associated with specific ATP release mechanisms and involves tyrosine kinases, mitogen-activated protein kinases, WNKs and Ste20-related kinases that are modulated by osmotic stress and cell volume perturbations.
| Originalsprog | Engelsk |
|---|---|
| Titel | Ion channels and transporters of epithelia in health and disease |
| Redaktører | Kirk L. Hamiltion, Daniel C. Devor |
| Antal sider | 55 |
| Vol/bind | Part 1 |
| Forlag | Springer |
| Publikationsdato | 2016 |
| Sider | 131-185 |
| Kapitel | 4 |
| ISBN (Trykt) | 978-1-4939-3364-8 |
| ISBN (Elektronisk) | 978-1-4939-3366-2 |
| DOI | |
| Status | Udgivet - 2016 |
| Navn | Physiology in Health and Disease |
|---|