Limits...
L-citrulline for protection of endothelial function from ADMA-induced injury in porcine coronary artery.

Xuan C, Lun LM, Zhao JX, Wang HW, Wang J, Ning CP, Liu Z, Zhang BB, He GW - Sci Rep (2015)

Bottom Line: Expression of eNOS, p-eNOS(ser1177), and ASS in PCA significantly increased after L-citrulline incubation.L-citrulline also markedly restored the NO production, and cGMP level which was reduced by ADMA.L-citrulline improves endothelium-dependent vasodilation through NO/ cGMP pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.

ABSTRACT
Endogenous nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a cardiovascular risk factor. We tested the hypothesis that L-citrulline may ameliorate the endothelial function altered by ADMA in porcine coronary artery (PCA). Myograph study for vasorelaxation, electrochemical measurement for NO, RT-PCR, and Western blot analysis for expression of eNOS, argininosuccinate synthetase (ASS), and p-eNOS(ser1177) were performed. cGMP was determined by enzyme immunoassay. Superoxide anion (O2.(-)) production was detected by the lucigenin-enhanced chemiluminescence method. Compare with controls (96.03% ± 6.2%), the maximal relaxation induced by bradykinin was significantly attenuated (61.55% ± 4.8%, p<0.01), and significantly restored by L-citrulline (82.67 ± 6.4%, p<0.05) after 24 hours of ADMA exposure. Expression of eNOS, p-eNOS(ser1177), and ASS in PCA significantly increased after L-citrulline incubation. L-citrulline also markedly restored the NO production, and cGMP level which was reduced by ADMA. The increased O2.(-) production by ADMA was also inhibited by L-citrulline. L-citrulline restores the endothelial function in preparations treated with ADMA by preservation of NO production and suppression of O2.(-) generation. Preservation of NO is attributed to the upregulation of eNOS expression along with activation of p-eNOS(ser1177). L-citrulline improves endothelium-dependent vasodilation through NO/ cGMP pathway.

No MeSH data available.


Related in: MedlinePlus

The BK-induced relaxation in porcine coronary artery (PCA) was endothelium dependent.The BK-induced relaxation was abolished in PCA rings without endothelium (E-). L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings. Data are shown as mean ± SEM. (**p < 0.01, vs. control group. n = 9, two-way ANOVA).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4457144&req=5

f1: The BK-induced relaxation in porcine coronary artery (PCA) was endothelium dependent.The BK-induced relaxation was abolished in PCA rings without endothelium (E-). L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings. Data are shown as mean ± SEM. (**p < 0.01, vs. control group. n = 9, two-way ANOVA).

Mentions: The BK-mediated relaxation was abolished in the endothelium-denuded rings (Fig. 1). This result showed that the BK-induced relaxation in our experiments was endothelium dependent. In addition, the L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings (Fig. 1).


L-citrulline for protection of endothelial function from ADMA-induced injury in porcine coronary artery.

Xuan C, Lun LM, Zhao JX, Wang HW, Wang J, Ning CP, Liu Z, Zhang BB, He GW - Sci Rep (2015)

The BK-induced relaxation in porcine coronary artery (PCA) was endothelium dependent.The BK-induced relaxation was abolished in PCA rings without endothelium (E-). L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings. Data are shown as mean ± SEM. (**p < 0.01, vs. control group. n = 9, two-way ANOVA).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4457144&req=5

f1: The BK-induced relaxation in porcine coronary artery (PCA) was endothelium dependent.The BK-induced relaxation was abolished in PCA rings without endothelium (E-). L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings. Data are shown as mean ± SEM. (**p < 0.01, vs. control group. n = 9, two-way ANOVA).
Mentions: The BK-mediated relaxation was abolished in the endothelium-denuded rings (Fig. 1). This result showed that the BK-induced relaxation in our experiments was endothelium dependent. In addition, the L-citrulline had no effect of improving relaxation in the endothelium-denuded PCA rings (Fig. 1).

Bottom Line: Expression of eNOS, p-eNOS(ser1177), and ASS in PCA significantly increased after L-citrulline incubation.L-citrulline also markedly restored the NO production, and cGMP level which was reduced by ADMA.L-citrulline improves endothelium-dependent vasodilation through NO/ cGMP pathway.

View Article: PubMed Central - PubMed

Affiliation: Department of Clinical Laboratory, The Affiliated Hospital of Qingdao University, Qingdao, China.

ABSTRACT
Endogenous nitric oxide synthase (eNOS) inhibitor asymmetric dimethylarginine (ADMA) is a cardiovascular risk factor. We tested the hypothesis that L-citrulline may ameliorate the endothelial function altered by ADMA in porcine coronary artery (PCA). Myograph study for vasorelaxation, electrochemical measurement for NO, RT-PCR, and Western blot analysis for expression of eNOS, argininosuccinate synthetase (ASS), and p-eNOS(ser1177) were performed. cGMP was determined by enzyme immunoassay. Superoxide anion (O2.(-)) production was detected by the lucigenin-enhanced chemiluminescence method. Compare with controls (96.03% ± 6.2%), the maximal relaxation induced by bradykinin was significantly attenuated (61.55% ± 4.8%, p<0.01), and significantly restored by L-citrulline (82.67 ± 6.4%, p<0.05) after 24 hours of ADMA exposure. Expression of eNOS, p-eNOS(ser1177), and ASS in PCA significantly increased after L-citrulline incubation. L-citrulline also markedly restored the NO production, and cGMP level which was reduced by ADMA. The increased O2.(-) production by ADMA was also inhibited by L-citrulline. L-citrulline restores the endothelial function in preparations treated with ADMA by preservation of NO production and suppression of O2.(-) generation. Preservation of NO is attributed to the upregulation of eNOS expression along with activation of p-eNOS(ser1177). L-citrulline improves endothelium-dependent vasodilation through NO/ cGMP pathway.

No MeSH data available.


Related in: MedlinePlus