Limits...
P2X receptors trigger intracellular alkalization in isolated perfused mouse medullary thick ascending limb.

de Bruijn PI, Bleich M, Praetorius HA, Leipziger J - Acta Physiol (Oxf) (2014)

Bottom Line: The renal outer medullary K(+) channel (ROMK) is sensitive to intracellular pH where a reduction leads to closing of ROMK.We speculated that P2X receptor stimulation in the TAL could lead to changes in pHi , leading to a reduction in NaCl transport.This increased NHE3 activity causes H(+) secretion in the mTAL and provides further support that the TAL is a site of urinary acidification.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedicine, Physiology and Biophysics, Aarhus University, Aarhus C, Denmark.

Show MeSH

Related in: MedlinePlus

Luminal furosemide inhibits the basolateral ATP-induced alkalization. (a) Original trace of an experiment, where ATP (100 μm) is added to the bath in the presence of luminal furosemide (100 μm). (b) Summary (ΔpHi) of the data, n = 6. *Indicates statistical significance, P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4374443&req=5

fig06: Luminal furosemide inhibits the basolateral ATP-induced alkalization. (a) Original trace of an experiment, where ATP (100 μm) is added to the bath in the presence of luminal furosemide (100 μm). (b) Summary (ΔpHi) of the data, n = 6. *Indicates statistical significance, P < 0.001.

Mentions: Furosemide and ATP both cause significant intracellular alkalizations in mTAL that require NHE3 activity (this study and de Bruijn et al. 2013), and they are known to reduce tubular transport in this segment (Greger 1985, Marques et al. 2012). It was therefore interesting to study whether the pHi effects of the two substances are additive. Figure6a illustrates that furosemide causes a marked intracellular alkalization from pH 7.25 ± 0.08 to pH 7.60 ± 0.02 (n = 6, Fig.6b). When basolateral ATP (100 μm) was added during the continuous presence of luminal furosemide, pHi remained unchanged. These results do not support an additive effect of these two alkalizing stimuli and thus are consistent with the notion of a common underlying cause.


P2X receptors trigger intracellular alkalization in isolated perfused mouse medullary thick ascending limb.

de Bruijn PI, Bleich M, Praetorius HA, Leipziger J - Acta Physiol (Oxf) (2014)

Luminal furosemide inhibits the basolateral ATP-induced alkalization. (a) Original trace of an experiment, where ATP (100 μm) is added to the bath in the presence of luminal furosemide (100 μm). (b) Summary (ΔpHi) of the data, n = 6. *Indicates statistical significance, P < 0.001.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4374443&req=5

fig06: Luminal furosemide inhibits the basolateral ATP-induced alkalization. (a) Original trace of an experiment, where ATP (100 μm) is added to the bath in the presence of luminal furosemide (100 μm). (b) Summary (ΔpHi) of the data, n = 6. *Indicates statistical significance, P < 0.001.
Mentions: Furosemide and ATP both cause significant intracellular alkalizations in mTAL that require NHE3 activity (this study and de Bruijn et al. 2013), and they are known to reduce tubular transport in this segment (Greger 1985, Marques et al. 2012). It was therefore interesting to study whether the pHi effects of the two substances are additive. Figure6a illustrates that furosemide causes a marked intracellular alkalization from pH 7.25 ± 0.08 to pH 7.60 ± 0.02 (n = 6, Fig.6b). When basolateral ATP (100 μm) was added during the continuous presence of luminal furosemide, pHi remained unchanged. These results do not support an additive effect of these two alkalizing stimuli and thus are consistent with the notion of a common underlying cause.

Bottom Line: The renal outer medullary K(+) channel (ROMK) is sensitive to intracellular pH where a reduction leads to closing of ROMK.We speculated that P2X receptor stimulation in the TAL could lead to changes in pHi , leading to a reduction in NaCl transport.This increased NHE3 activity causes H(+) secretion in the mTAL and provides further support that the TAL is a site of urinary acidification.

View Article: PubMed Central - PubMed

Affiliation: Department of Biomedicine, Physiology and Biophysics, Aarhus University, Aarhus C, Denmark.

Show MeSH
Related in: MedlinePlus