ArticleThe Journal of physiology2003
Hypotonic stimulation of the Na+ active transport in frog skeletal muscle: role of the cytoskeleton.
Article in The Journal of physiology, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 10 citations in OpenAlex.
- The sodium-calcium exchanger is a mechanosensitive transporter.The Journal of physiology · 2008Article
- Dynamic effects of Hg2+-induced changes in cell volume.Cell biochemistry and biophysics · 2008Article
- Dual control of cardiac Na+ Ca2+ exchange by PIP(2): analysis of the surface membrane fraction by extracellular cysteine PEGylation.The Journal of physiology · 2007Article
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1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypotonicity produces a marked activation of the Na+ pump in frog sartorius muscle. The increase in net Na+ efflux under hypotonic conditions occurs despite the reductions in [Na+]i that are due to fibre swelling and Na+ loss. The pump density (ouabain binding) increases not only upon reduction of the medium osmotic pressure (pi) from its normal value (pi = 1) to one-half (pi = 0.5), but also in muscles that are returned to pi = 1 after equilibration in pi = 2 medium. The equilibration in pi = 2 medium does not affect pump density. Ouabain-binding increments cannot be ascribed to a rise in the Na+-K+ exchange rate of a fixed number of pumps: they also occurred in the continued presence of a saturating concentration of ouabain (50 microM). Under those conditions, the pi = 1 pi = 0.5 transfer produced a 43 % increase in pump sites, while the pi = 2 pi = 1 transfer induced a rise of 46 %. Actinomycin D did not alter the stimulation of Na+ extrusion elicited by hypotonicity, suggesting that de novo synthesis of pumps was not involved in the increase of the apparent number of pump sites. Disruption of microtubules by colchicine (100 microM) and intermediate filaments by acrylamide (4 mM) did not alter the hypotonic effect. Likewise, genistein (100 microM), a specific inhibitor of tyrosine kinase, did not affect significantly the hypotonic response. Microfilament-disrupting agents like cytochalasin B (5 microM) and latrunculin B (10 microM) reduced the increase in Na+ efflux induced by pi = 1 pi = 0.5 transfer by about 35 % and 72 %, respectively. Latrunculin B reduced the increases in pump density generated by pi = 1 pi = 0.5 and pi = 2 pi = 1 transfers by about 79 % and 91 %, respectively. The results suggest that the membrane stretch due to hypotonic fibre volume increase would promote a microfilament-mediated insertion of submembranous spare Na+ pumps in the sarcolemma and, consequently, the rise in active Na+ transport.
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