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Nitric Oxide Protects L-Type Calcium Channel of Cardiomyocyte during Long-Term Isoproterenol Stimulation in Tail-Suspended Rats.

Yue ZJ, Xu PT, Jiao B, Chang H, Song Z, Xie MJ, Yu ZB - Biomed Res Int (2015)

Bottom Line: Expression and activity of nNOS as well as S-nitrosylation of LTCC α1C subunit significantly decreased in the myocardium of SUS rats.Specific inhibitor NAAN of nNOS reduced maximal I Ca,L to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal I Ca,L in SUS group to similar extent of CON group after 50 min of ISO treatment.In conclusion, NO-induced S-nitrosylation of LTCC α1C subunit may competitively prevent oxidation from ROS at the same sites.

View Article: PubMed Central - PubMed

Affiliation: Department of Aerospace Physiology, Fourth Military Medical University, No. 169 Changlexi Road, Xi'an 710032, China.

ABSTRACT
The aim of this study was to investigate the effects of nitric oxide (NO) and reactive oxygen species (ROS) on L-type calcium channel (LTCC) gating properties of cardiomyocytes during long-term isoproterenol (ISO) stimulation. Expression and activity of nNOS as well as S-nitrosylation of LTCC α1C subunit significantly decreased in the myocardium of SUS rats. Long-term ISO stimulation increased ROS in cardiomyocytes of SUS rats. ISO-enhanced calcium current (I Ca,L) in the SUS group was less than that in the CON group. The maximal I Ca,L decreased to about 80% or 60% of initial value at the 50th minute of ISO treatment in CON or SUS group, respectively. Specific inhibitor NAAN of nNOS reduced maximal I Ca,L to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal I Ca,L in SUS group to similar extent of CON group after 50 min of ISO treatment. Long-term ISO stimulation also changed steady-state activation (P < 0.01), inactivation (P < 0.01), and recovery (P < 0.05) characteristics of LTCC in SUS group. In conclusion, NO-induced S-nitrosylation of LTCC α1C subunit may competitively prevent oxidation from ROS at the same sites. Furthermore, LTCC can be protected by NO during long-term ISO stimulation.

No MeSH data available.


Related in: MedlinePlus

I-V curves in left ventricular cardiomyocyte of CON and SUS rats. (a) I-V curves of the CON and 4 wk SUS groups with or without 1 μM of ISO stimulation. (b) The increasing percentage of peak ICa,L with 1 μM of ISO treatment for 10 min. (c) I-V curves of LTCC with or without 240 nM nNOS inhibitor (NAAN). (d) I-V curves of LTCC with or without 240 nM NAAN + 1 μM ISO treatment. (e) I-V curves of LTCC with or without 100 μM NO donor (SNAP) treatment. (f) I-V curves of LTCC with or without 100 μM SNAP + 1 μM ISO treatment. (g) Maximal ICa,L of I-V curves with different treatments. (h) Ratios of peak ICa,L at the 50th min with ISO treatment to that at the 10th min. Data are mean ± SEM; n = 6 cardiomyocytes from 5 hearts in each treatment. ∗P < 0.05 and ∗∗P < 0.01 versus CON vehicle. #P < 0.05 and ##P < 0.01 versus CON with ISO treatment. &P < 0.05 and &&P < 0.01 versus the value at the 10th min.
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fig4: I-V curves in left ventricular cardiomyocyte of CON and SUS rats. (a) I-V curves of the CON and 4 wk SUS groups with or without 1 μM of ISO stimulation. (b) The increasing percentage of peak ICa,L with 1 μM of ISO treatment for 10 min. (c) I-V curves of LTCC with or without 240 nM nNOS inhibitor (NAAN). (d) I-V curves of LTCC with or without 240 nM NAAN + 1 μM ISO treatment. (e) I-V curves of LTCC with or without 100 μM NO donor (SNAP) treatment. (f) I-V curves of LTCC with or without 100 μM SNAP + 1 μM ISO treatment. (g) Maximal ICa,L of I-V curves with different treatments. (h) Ratios of peak ICa,L at the 50th min with ISO treatment to that at the 10th min. Data are mean ± SEM; n = 6 cardiomyocytes from 5 hearts in each treatment. ∗P < 0.05 and ∗∗P < 0.01 versus CON vehicle. #P < 0.05 and ##P < 0.01 versus CON with ISO treatment. &P < 0.05 and &&P < 0.01 versus the value at the 10th min.

Mentions: The voltage dependence of ICa,L activation showed a left shift in the SUS group as compared with the CON group under the basic condition. ISO increased maximal ICa,L in the CON and SUS groups and only induced a left shift in the CON group (Figures 4(a) and 4(g)). The percent increase in the maximal amplitude of ICa,L in the CON group was greater than that in the 4 wk SUS group after ISO stimulation (P < 0.05, Figure 4(b)). Under the NAAN treatment, the maximal ICa,L significantly increased in the CON and SUS group (P < 0.05, Figures 4(c) and 4(g)); ISO induced less enhancement in the maximal ICa,L and did not shift the I-V curves in the CON and SUS groups (P < 0.01, Figures 4(d) and 4(g)). SNAP decreased maximal ICa,L in the CON and SUS groups but did not influence I-V curves (P < 0.01, Figures 4(e) and 4(g)). ISO also induced less enhancement in the maximal ICa,L during SNAP treatment in the CON and SUS groups (P < 0.05, Figures 4(f) and 4(g)).


Nitric Oxide Protects L-Type Calcium Channel of Cardiomyocyte during Long-Term Isoproterenol Stimulation in Tail-Suspended Rats.

Yue ZJ, Xu PT, Jiao B, Chang H, Song Z, Xie MJ, Yu ZB - Biomed Res Int (2015)

I-V curves in left ventricular cardiomyocyte of CON and SUS rats. (a) I-V curves of the CON and 4 wk SUS groups with or without 1 μM of ISO stimulation. (b) The increasing percentage of peak ICa,L with 1 μM of ISO treatment for 10 min. (c) I-V curves of LTCC with or without 240 nM nNOS inhibitor (NAAN). (d) I-V curves of LTCC with or without 240 nM NAAN + 1 μM ISO treatment. (e) I-V curves of LTCC with or without 100 μM NO donor (SNAP) treatment. (f) I-V curves of LTCC with or without 100 μM SNAP + 1 μM ISO treatment. (g) Maximal ICa,L of I-V curves with different treatments. (h) Ratios of peak ICa,L at the 50th min with ISO treatment to that at the 10th min. Data are mean ± SEM; n = 6 cardiomyocytes from 5 hearts in each treatment. ∗P < 0.05 and ∗∗P < 0.01 versus CON vehicle. #P < 0.05 and ##P < 0.01 versus CON with ISO treatment. &P < 0.05 and &&P < 0.01 versus the value at the 10th min.
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Related In: Results  -  Collection

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fig4: I-V curves in left ventricular cardiomyocyte of CON and SUS rats. (a) I-V curves of the CON and 4 wk SUS groups with or without 1 μM of ISO stimulation. (b) The increasing percentage of peak ICa,L with 1 μM of ISO treatment for 10 min. (c) I-V curves of LTCC with or without 240 nM nNOS inhibitor (NAAN). (d) I-V curves of LTCC with or without 240 nM NAAN + 1 μM ISO treatment. (e) I-V curves of LTCC with or without 100 μM NO donor (SNAP) treatment. (f) I-V curves of LTCC with or without 100 μM SNAP + 1 μM ISO treatment. (g) Maximal ICa,L of I-V curves with different treatments. (h) Ratios of peak ICa,L at the 50th min with ISO treatment to that at the 10th min. Data are mean ± SEM; n = 6 cardiomyocytes from 5 hearts in each treatment. ∗P < 0.05 and ∗∗P < 0.01 versus CON vehicle. #P < 0.05 and ##P < 0.01 versus CON with ISO treatment. &P < 0.05 and &&P < 0.01 versus the value at the 10th min.
Mentions: The voltage dependence of ICa,L activation showed a left shift in the SUS group as compared with the CON group under the basic condition. ISO increased maximal ICa,L in the CON and SUS groups and only induced a left shift in the CON group (Figures 4(a) and 4(g)). The percent increase in the maximal amplitude of ICa,L in the CON group was greater than that in the 4 wk SUS group after ISO stimulation (P < 0.05, Figure 4(b)). Under the NAAN treatment, the maximal ICa,L significantly increased in the CON and SUS group (P < 0.05, Figures 4(c) and 4(g)); ISO induced less enhancement in the maximal ICa,L and did not shift the I-V curves in the CON and SUS groups (P < 0.01, Figures 4(d) and 4(g)). SNAP decreased maximal ICa,L in the CON and SUS groups but did not influence I-V curves (P < 0.01, Figures 4(e) and 4(g)). ISO also induced less enhancement in the maximal ICa,L during SNAP treatment in the CON and SUS groups (P < 0.05, Figures 4(f) and 4(g)).

Bottom Line: Expression and activity of nNOS as well as S-nitrosylation of LTCC α1C subunit significantly decreased in the myocardium of SUS rats.Specific inhibitor NAAN of nNOS reduced maximal I Ca,L to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal I Ca,L in SUS group to similar extent of CON group after 50 min of ISO treatment.In conclusion, NO-induced S-nitrosylation of LTCC α1C subunit may competitively prevent oxidation from ROS at the same sites.

View Article: PubMed Central - PubMed

Affiliation: Department of Aerospace Physiology, Fourth Military Medical University, No. 169 Changlexi Road, Xi'an 710032, China.

ABSTRACT
The aim of this study was to investigate the effects of nitric oxide (NO) and reactive oxygen species (ROS) on L-type calcium channel (LTCC) gating properties of cardiomyocytes during long-term isoproterenol (ISO) stimulation. Expression and activity of nNOS as well as S-nitrosylation of LTCC α1C subunit significantly decreased in the myocardium of SUS rats. Long-term ISO stimulation increased ROS in cardiomyocytes of SUS rats. ISO-enhanced calcium current (I Ca,L) in the SUS group was less than that in the CON group. The maximal I Ca,L decreased to about 80% or 60% of initial value at the 50th minute of ISO treatment in CON or SUS group, respectively. Specific inhibitor NAAN of nNOS reduced maximal I Ca,L to 50% of initial value in the CON group; in contrast, NO donor SNAP maintained maximal I Ca,L in SUS group to similar extent of CON group after 50 min of ISO treatment. Long-term ISO stimulation also changed steady-state activation (P < 0.01), inactivation (P < 0.01), and recovery (P < 0.05) characteristics of LTCC in SUS group. In conclusion, NO-induced S-nitrosylation of LTCC α1C subunit may competitively prevent oxidation from ROS at the same sites. Furthermore, LTCC can be protected by NO during long-term ISO stimulation.

No MeSH data available.


Related in: MedlinePlus