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Understanding the physiology of the asymptomatic diaphragm of the M1592V hyperkalemic periodic paralysis mouse.

Ammar T, Lin W, Higgins A, Hayward LJ, Renaud JM - J. Gen. Physiol. (2015)

Bottom Line: The improved resting membrane potential (EM) results from significantly increased Na(+) K(+) pump electrogenic activity, and not from an increased protein content.One suggested mechanism for the greater action potential amplitude is lower intracellular Na(+) concentration because of greater Na(+) K(+) pump activity, allowing better Na(+) current during the action potential depolarization phase.Finally, HyperKPP diaphragm had a greater capacity to generate force at depolarized EM compared with wild-type diaphragm.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.

No MeSH data available.


Related in: MedlinePlus

The NKA electrogenic contribution at 4.7 mM K+ was significantly greater in the HyperKPP diaphragm than in the EDL and soleus. (A) Total NKA electrogenic contribution calculated from the difference in resting EM in the absence and presence of 100 µM ouabain, which fully inhibits NKAα1 and NKAα2 activity. (B) NKAα2 electrogenic contribution calculated from the difference in resting EM in the absence and presence of 1 µM ouabain, which reduced the activity of NKAα2 by 92% and that of NKAα1 by 6%. (C) NKAα1 electrogenic contribution calculated from the difference in total and NKAα2 electrogenic contribution. Error bars represent the SEM for the number of fibers and muscles given in Fig. 8. *, mean electrogenic contribution in HyperKPP was significantly different from the mean value for wild type; ANOVA and LSD; P < 0.05.
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fig10: The NKA electrogenic contribution at 4.7 mM K+ was significantly greater in the HyperKPP diaphragm than in the EDL and soleus. (A) Total NKA electrogenic contribution calculated from the difference in resting EM in the absence and presence of 100 µM ouabain, which fully inhibits NKAα1 and NKAα2 activity. (B) NKAα2 electrogenic contribution calculated from the difference in resting EM in the absence and presence of 1 µM ouabain, which reduced the activity of NKAα2 by 92% and that of NKAα1 by 6%. (C) NKAα1 electrogenic contribution calculated from the difference in total and NKAα2 electrogenic contribution. Error bars represent the SEM for the number of fibers and muscles given in Fig. 8. *, mean electrogenic contribution in HyperKPP was significantly different from the mean value for wild type; ANOVA and LSD; P < 0.05.

Mentions: The total electrogenic contribution of NKAα1 and NKAα2, calculated from the differences in resting EM in the absence and presence of 100 µM ouabain, was 19–21 mV in wild-type muscles and was not significantly different from the 18–23-mV contribution in the HyperKPP soleus and EDL (Fig. 10 A). In the HyperKPP diaphragm, however, the total NKA contribution was significantly greater at 32 mV compared with only 19 mV in the wild-type diaphragm. The NKAα2 electrogenic contribution, calculated from the depolarization caused by 1 µM ouabain, was similar in wild-type and HyperKPP soleus and higher in the HyperKPP EDL and diaphragm than in their wild-type counterparts, even though the differences were not significant (Fig. 10 B). The NKAα1 electrogenic contribution, or the difference between total and NKAα2 contribution, was not different between wild-type and HyperKPP EDL and soleus, whereas it was significantly greater in HyperKPP than in the wild-type diaphragm (Fig. 10 C).


Understanding the physiology of the asymptomatic diaphragm of the M1592V hyperkalemic periodic paralysis mouse.

Ammar T, Lin W, Higgins A, Hayward LJ, Renaud JM - J. Gen. Physiol. (2015)

The NKA electrogenic contribution at 4.7 mM K+ was significantly greater in the HyperKPP diaphragm than in the EDL and soleus. (A) Total NKA electrogenic contribution calculated from the difference in resting EM in the absence and presence of 100 µM ouabain, which fully inhibits NKAα1 and NKAα2 activity. (B) NKAα2 electrogenic contribution calculated from the difference in resting EM in the absence and presence of 1 µM ouabain, which reduced the activity of NKAα2 by 92% and that of NKAα1 by 6%. (C) NKAα1 electrogenic contribution calculated from the difference in total and NKAα2 electrogenic contribution. Error bars represent the SEM for the number of fibers and muscles given in Fig. 8. *, mean electrogenic contribution in HyperKPP was significantly different from the mean value for wild type; ANOVA and LSD; P < 0.05.
© Copyright Policy - openaccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4664826&req=5

fig10: The NKA electrogenic contribution at 4.7 mM K+ was significantly greater in the HyperKPP diaphragm than in the EDL and soleus. (A) Total NKA electrogenic contribution calculated from the difference in resting EM in the absence and presence of 100 µM ouabain, which fully inhibits NKAα1 and NKAα2 activity. (B) NKAα2 electrogenic contribution calculated from the difference in resting EM in the absence and presence of 1 µM ouabain, which reduced the activity of NKAα2 by 92% and that of NKAα1 by 6%. (C) NKAα1 electrogenic contribution calculated from the difference in total and NKAα2 electrogenic contribution. Error bars represent the SEM for the number of fibers and muscles given in Fig. 8. *, mean electrogenic contribution in HyperKPP was significantly different from the mean value for wild type; ANOVA and LSD; P < 0.05.
Mentions: The total electrogenic contribution of NKAα1 and NKAα2, calculated from the differences in resting EM in the absence and presence of 100 µM ouabain, was 19–21 mV in wild-type muscles and was not significantly different from the 18–23-mV contribution in the HyperKPP soleus and EDL (Fig. 10 A). In the HyperKPP diaphragm, however, the total NKA contribution was significantly greater at 32 mV compared with only 19 mV in the wild-type diaphragm. The NKAα2 electrogenic contribution, calculated from the depolarization caused by 1 µM ouabain, was similar in wild-type and HyperKPP soleus and higher in the HyperKPP EDL and diaphragm than in their wild-type counterparts, even though the differences were not significant (Fig. 10 B). The NKAα1 electrogenic contribution, or the difference between total and NKAα2 contribution, was not different between wild-type and HyperKPP EDL and soleus, whereas it was significantly greater in HyperKPP than in the wild-type diaphragm (Fig. 10 C).

Bottom Line: The improved resting membrane potential (EM) results from significantly increased Na(+) K(+) pump electrogenic activity, and not from an increased protein content.One suggested mechanism for the greater action potential amplitude is lower intracellular Na(+) concentration because of greater Na(+) K(+) pump activity, allowing better Na(+) current during the action potential depolarization phase.Finally, HyperKPP diaphragm had a greater capacity to generate force at depolarized EM compared with wild-type diaphragm.

View Article: PubMed Central - HTML - PubMed

Affiliation: Department of Cellular and Molecular Medicine, University of Ottawa, Ottawa, Ontario K1H 8M5, Canada.

No MeSH data available.


Related in: MedlinePlus