ArticlePflugers Archiv : European journal of physiology1995
Regulatory volume decrease in a renal distal tubular cell line (A6). I. Role of K+ and Cl-.
Article in Pflugers Archiv : European journal of physiology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 25 citations in OpenAlex.
- ENaC, renal sodium excretion and extracellular ATP.Purinergic signalling · 2009Article
- Recovery of cell volume and electrolytes of A6 cells after re-establishing isotonicity following hypotonic stress.Pflugers Archiv : European journal of physiology · 2003Article
- External Ni2 + and ENaC in A6 cells: Na+ current stimulation by competition at a binding site for amiloride and Na+.The Journal of membrane biology · 2003Article
- Hypotonic treatment evokes biphasic ATP release across the basolateral membrane of cultured renal epithelia (A6).The Journal of physiology · 2002Article
- Activation of the Na+-K+ pump by hyposmolality through tyrosine kinase-dependent Cl- conductance in Xenopus renal epithelial A6 cells.The Journal of physiology · 1999Article
- Cross talk of bumetanide-sensitive and HCO3--dependent transporters activated by IBMX in renal epithelial A6 cells.The Journal of membrane biology · 1997Article
- Regulatory volume decrease in a renal distal tubular cell line (A6). II. Effect of Na+ transport rate.Pflugers Archiv : European journal of physiology · 1995Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Changes in volume of A6 epithelial cells were monitored by recording cell thickness (Tc). The response of Tc to a reduction of the basolateral osmolality from 260 to 140 mosmol/kg was recorded while transepithelial Na+ transport was inhibited by 20 microM amiloride. With Cl--containing bathing media, this osmotic challenge elicited a rapid rise in Tc followed by a regulatory volume decrease (RVD). Substitution of SO4(2-) or gluconate for Cl- markedly reduced the RVD, whereas cells completely maintained their ability to regulate their volume after replacing Cl- by NO3(-). A conductive pathway for Cl- excretion is suggested, which is insensitive to NPPB [5-nitro-2-(3-phenylpropylamino)benzoic acid], an inhibitor of some types of Cl- channels. Ba2+ (5 or 20 mM) reduced the RVD. A more pronounced inhibition of the RVD was obtained with 500 microM quinine, a potent blocker of volume-activated K+ channels. K+-induced depolarization of the basolateral membranes of tissues incubated with SO4(2-)-containing solutions completely abolished the RVD. Noise analysis in the presence of Ba2+ showed the activation of an apical K+ conductive pathway. These results demonstrate that cell volume regulation is controlled by processes involving Cl- and K+ excretion through conductive pathways.
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