Effects of changes in osmolarity on isolated human airways

Jongejan, R. C.; Jongste, Johan C. de; Raatgeep, R. C.; Bonta, I. L.; Kerrebijn, K. F.

doi:10.1152/jappl.1990.68.4.1568

Cited by 28 publications

(23 citation statements)

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“…8a,b). This fits with results obtained by Jongejan et al (1990) showing that 450 mOsm is the highest osmolarity that does not cause osmotic shrinkage. When the cells were allowed to recover in 295 mOsm EMEM for 1 hour subsequent to hyperosmotic stress at 700 mOsm, the morphological recovery was remarkable.…”

Section: Teer Measurementssupporting

confidence: 92%

Effects of hyperosmotic stress on cultured airway epithelial cells

et al. 2007

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Inhalation of hyperosmotic solutions (salt, mannitol) has been used in the treatment of patients with cystic fibrosis or asthma, but the mechanism behind the effect of hyperosmotic solutions is unclear. The relation between osmolarity and permeability changes was examined in an airway cell line by the addition of NaCl, NaBr, LiCl, mannitol, or xylitol (295-700 mOsm). Transepithelial resistance was measured as an indicator of the tightness of the cultures. Cell-cell contacts and morphology were investigated by immunofluorescence and by transmission electron microscopy, with lanthanum nitrate added to the luminal side of the epithelium to investigate tight junction permeability. The electrolyte solutions caused a significant decrease in transepithelial resistance from 450 mOsm upwards, when the hyperosmolar exposure was gradually increased from 295 to 700 mOsm; whereas the nonelectrolyte solutions caused a decrease in transepithelial resistance from 700 mOsm upwards. Old cultures reacted in a more rigid way compared to young cultures. Immuno-fluorescence pictures showed weaker staining for the proteins ZO-1, claudin-4, and plakoglobin in treated samples compared to the control. The ultrastructure revealed an increased number of open tight junctions as well as a disturbed morphology with increasing osmolarity, and electrolyte solutions opened a larger proportion of tight junctions than nonelectrolyte solutions. This study shows that hyperosmotic solutions cause the opening of tight junctions, which may increase the permeability of the paracellular pathway and result in increased transepithelial water transport.

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Section: Teer Measurementssupporting

confidence: 92%

Effects of hyperosmotic stress on cultured airway epithelial cells

et al. 2007

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“…In bronchial smooth muscle, similar observations about different modes of action of hyper-and hyposmolar solutions have also been reached [13]. In hyperosmolar solutions the changes to phasic and baseline tension were a function of osmolarity per se, as similar responses were observed irrespective of the osmolyte used, and were not accompanied by significant alterations to intracellular [Ca 2+ ] in isolated detrusor myocytes.…”

Section: Discussionsupporting

confidence: 63%

The actions of altered osmolarity on guinea-pig detrusor smooth muscle contractility and intracellular calcium

Proctor¹,

Fry²

1999

Pfl�gers Archiv European Journal of Physiology

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The study measured the effects in vitro of changing extracellular osmolarity on the contractility of detrusor smooth muscle strips. The data were interpreted in the context of separate measurements from isolated cells of alterations to the intracellular [Ca2+], [Ca2+]i. Increased osmolarity (300-700 mosmol l-1) reduced phasic contractions but increased resting tension regardless of whether sucrose, LiCl or NaCl were used as osmolytes. [Ca2+]i was decreased slightly only when NaCl increased osmolarity, otherwise it was unchanged. The contractile effects may be explained by tissue shrinkage and reduction of detrusor excitability. Lowered osmolarity (300-64 mosmol l-1) decreased phasic contractions but increased resting tension and [Ca2+]i. The raised resting tension was due solely to low osmolarity and was independent of changes to [Na], [Cl] or ionic strength. The rise of [Ca2+]i was due partly to Ca2+ influx through Na(+)-Ca2+ exchange but a fraction was independent of extracellular Ca, unaffected by Gd3+, and persisted in the presence of caffeine. By contrast, reduction of phasic tension was due mainly to the reduced ionic strength, not osmolarity. The results do not support the presence of functional stretch-activated channels and suggest only a minor role for Na(+)-Ca2+ exchange under these conditions. However, they do suggest an intracellular source of Ca2+, which is independent of the sarcoplasmic reticulum.

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“…It has been reported that hypotonic stimulation induces airway smooth muscle contraction in human airways in vivo and in vitro (2,3,11,20,31). In the present studies, we show that hypotonic solution-induced airway contraction is dependent on the extracellular Ca 2ϩ in both human and guinea pig airways.…”

Section: Discussionmentioning

confidence: 99%

“…Hypotonic solution also contracts isolated human airways (11,20). However, the mechanism for hypotonic stimulation-induced airway contraction is not clear.…”

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confidence: 99%

Functional TRPV4 channels are expressed in human airway smooth muscle cells

Jia¹,

Wang²,

Varty³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

164

128

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Hypotonic stimulation induces airway constriction in normal and asthmatic airways. However, the osmolarity sensor in the airway has not been characterized. TRPV4 (also known as VR-OAC, VRL-2, TRP12, OTRPC4), an osmotic-sensitive cation channel in the transient receptor potential (TRP) channel family, was recently cloned. In the present study, we show that TRPV4 mRNA was expressed in cultured human airway smooth muscle cells as analyzed by RT-PCR. Hypotonic stimulation induced Ca2+influx in human airway smooth muscle cells in an osmolarity-dependent manner, consistent with the reported biological activity of TRPV4 in transfected cells. In cultured muscle cells, 4α-phorbol 12,13-didecanoate (4-αPDD), a TRPV4 ligand, increased intracellular Ca2+level only when Ca2+was present in the extracellular solution. The 4-αPDD-induced Ca2+response was inhibited by ruthenium red (1 μM), a known TRPV4 inhibitor, but not by capsazepine (1 μM), a TRPV1 antagonist, indicating that 4-αPDD-induced Ca2+response is mediated by TRPV4. Verapamil (10 μM), an L-type voltage-gated Ca2+channel inhibitor, had no effect on the 4-αPDD-induced Ca2+response, excluding the involvement of L-type Ca2+channels. Furthermore, hypotonic stimulation elicited smooth muscle contraction through a mechanism dependent on membrane Ca2+channels in both isolated human and guinea pig airways. Hypotonicity-induced airway contraction was not inhibited by the L-type Ca2+channel inhibitor nifedipine (1 μM) or by the TRPV1 inhibitor capsazepine (1 μM). We conclude that functional TRPV4 is expressed in human airway smooth muscle cells and may act as an osmolarity sensor in the airway.

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Effects of changes in osmolarity on isolated human airways

Cited by 28 publications

References 0 publications

Effects of hyperosmotic stress on cultured airway epithelial cells

Effects of hyperosmotic stress on cultured airway epithelial cells

The actions of altered osmolarity on guinea-pig detrusor smooth muscle contractility and intracellular calcium

Functional TRPV4 channels are expressed in human airway smooth muscle cells

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