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CNP-pGC-cGMP-PDE3-cAMP Signal Pathway Upregulated in Gastric Smooth Muscle of Diabetic Rats.

Cai YL, Zhang MH, Huang X, Jiang JZ, Piao LH, Jin Z, Xu WX - Gastroenterol Res Pract (2015)

Bottom Line: The results demonstrated that the inhibitory effect of CNP on the spontaneous contraction of gastric antral circular smooth muscle was potentiated in STZ-induced diabetic rat.The expression of PDE3 is downregulated while the levels of gene expression of PDE1, PDE2, PDE4, and PDE5 were not altered in the diabetic gastric smooth muscle tissue.The results suggest that the sensitivity of gastric smooth muscle to CNP is potentiated via activation of CNP-pGC-cGMP-PDE3-cAMP signal pathway in STZ-induced diabetic rats, which may be associated with diabetes-induced gastric motility disorder.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Yanbian University School of Medicine, 977 Gongyuan Road, Yanji, Jilin 133002, China.

ABSTRACT
Our previous studies have shown that CNP-NPR-B/pGC-cGMP is upregulated in the diabetic rats. The present study was designed to determine whether the upregulation of CNP-NPR-B/pGC-cGMP signal pathway affects cGMP-PDE3-cAMP signal pathway in diabetic gastric smooth muscle. The gastric smooth muscle motility was observed by using isometric measurement. PDEs expressions in diabetic gastric smooth muscle tissue were observed by using immunohistochemistry, Western blotting, and RT-PCR methods. The results demonstrated that the inhibitory effect of CNP on the spontaneous contraction of gastric antral circular smooth muscle was potentiated in STZ-induced diabetic rat. CNP-induced increase of cGMP and cAMP was much higher in diabetic gastric smooth muscle tissue than in controls. The expression of PDE3 is downregulated while the levels of gene expression of PDE1, PDE2, PDE4, and PDE5 were not altered in the diabetic gastric smooth muscle tissue. The results suggest that the sensitivity of gastric smooth muscle to CNP is potentiated via activation of CNP-pGC-cGMP-PDE3-cAMP signal pathway in STZ-induced diabetic rats, which may be associated with diabetes-induced gastric motility disorder.

No MeSH data available.


Related in: MedlinePlus

Effect of CNP on the spontaneous contraction of gastric antral smooth muscle in control and diabetic rats. (a) CNP significantly inhibited the spontaneous contraction of gastric antral smooth muscle in both control and diabetic rats. (b) CNP caused significantly more inhibition on the amplitude of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (c) CNP caused significantly more inhibition on the frequency of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (d) CNP decreased the basal tension, which was more significant in diabetic rats than in controls (n = 8, P < 0.01). (e) The duration of CNP-induced inhibition of gastric smooth muscle contraction was significantly longer in diabetic rats than in controls (n = 8, P < 0.01).
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fig1: Effect of CNP on the spontaneous contraction of gastric antral smooth muscle in control and diabetic rats. (a) CNP significantly inhibited the spontaneous contraction of gastric antral smooth muscle in both control and diabetic rats. (b) CNP caused significantly more inhibition on the amplitude of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (c) CNP caused significantly more inhibition on the frequency of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (d) CNP decreased the basal tension, which was more significant in diabetic rats than in controls (n = 8, P < 0.01). (e) The duration of CNP-induced inhibition of gastric smooth muscle contraction was significantly longer in diabetic rats than in controls (n = 8, P < 0.01).

Mentions: After equilibration, spontaneous contractions of gastric antral circular smooth muscle from both control and diabetic rats were recorded. CNP (0.1 μmol/L) significantly inhibited the spontaneous contractions in both control and diabetic rats; however, the inhibitory response to CNP was much stronger in diabetic group (Figure 1(a)). CNP (0.1 μmol/L) inhibited the amplitudes of the contraction by 57.92  ±  4.66% in control rats and 80.15  ±  3.10% in diabetic rats (Figure 1(b), n = 8, P < 0.01). CNP (0.1 μmol/L) inhibited the frequencies of the contraction by 25.85 ± 6.57% in controls and 54.37 ± 5.35% in diabetic rats (Figure 1(c), n = 8, P < 0.01). Meanwhile, the tensions were significantly decreased to 47.88 ± 3.62 and 70.05 ± 3.21 after the administration of CNP in normal and diabetic groups, respectively (Figure 1(d), n = 8, P < 0.01). The durations of CNP-induced inhibition were 1.52 ± 0.50 min in control and 8.98 ± 0.88 min in diabetic group (Figure 1(e), n = 8, P < 0.01). The results suggest that the inhibitory effect of CNP on spontaneous contraction is potentiated in diabetic rats.


CNP-pGC-cGMP-PDE3-cAMP Signal Pathway Upregulated in Gastric Smooth Muscle of Diabetic Rats.

Cai YL, Zhang MH, Huang X, Jiang JZ, Piao LH, Jin Z, Xu WX - Gastroenterol Res Pract (2015)

Effect of CNP on the spontaneous contraction of gastric antral smooth muscle in control and diabetic rats. (a) CNP significantly inhibited the spontaneous contraction of gastric antral smooth muscle in both control and diabetic rats. (b) CNP caused significantly more inhibition on the amplitude of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (c) CNP caused significantly more inhibition on the frequency of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (d) CNP decreased the basal tension, which was more significant in diabetic rats than in controls (n = 8, P < 0.01). (e) The duration of CNP-induced inhibition of gastric smooth muscle contraction was significantly longer in diabetic rats than in controls (n = 8, P < 0.01).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4390109&req=5

fig1: Effect of CNP on the spontaneous contraction of gastric antral smooth muscle in control and diabetic rats. (a) CNP significantly inhibited the spontaneous contraction of gastric antral smooth muscle in both control and diabetic rats. (b) CNP caused significantly more inhibition on the amplitude of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (c) CNP caused significantly more inhibition on the frequency of the contraction in diabetic rats than in controls (n = 8, P < 0.01). (d) CNP decreased the basal tension, which was more significant in diabetic rats than in controls (n = 8, P < 0.01). (e) The duration of CNP-induced inhibition of gastric smooth muscle contraction was significantly longer in diabetic rats than in controls (n = 8, P < 0.01).
Mentions: After equilibration, spontaneous contractions of gastric antral circular smooth muscle from both control and diabetic rats were recorded. CNP (0.1 μmol/L) significantly inhibited the spontaneous contractions in both control and diabetic rats; however, the inhibitory response to CNP was much stronger in diabetic group (Figure 1(a)). CNP (0.1 μmol/L) inhibited the amplitudes of the contraction by 57.92  ±  4.66% in control rats and 80.15  ±  3.10% in diabetic rats (Figure 1(b), n = 8, P < 0.01). CNP (0.1 μmol/L) inhibited the frequencies of the contraction by 25.85 ± 6.57% in controls and 54.37 ± 5.35% in diabetic rats (Figure 1(c), n = 8, P < 0.01). Meanwhile, the tensions were significantly decreased to 47.88 ± 3.62 and 70.05 ± 3.21 after the administration of CNP in normal and diabetic groups, respectively (Figure 1(d), n = 8, P < 0.01). The durations of CNP-induced inhibition were 1.52 ± 0.50 min in control and 8.98 ± 0.88 min in diabetic group (Figure 1(e), n = 8, P < 0.01). The results suggest that the inhibitory effect of CNP on spontaneous contraction is potentiated in diabetic rats.

Bottom Line: The results demonstrated that the inhibitory effect of CNP on the spontaneous contraction of gastric antral circular smooth muscle was potentiated in STZ-induced diabetic rat.The expression of PDE3 is downregulated while the levels of gene expression of PDE1, PDE2, PDE4, and PDE5 were not altered in the diabetic gastric smooth muscle tissue.The results suggest that the sensitivity of gastric smooth muscle to CNP is potentiated via activation of CNP-pGC-cGMP-PDE3-cAMP signal pathway in STZ-induced diabetic rats, which may be associated with diabetes-induced gastric motility disorder.

View Article: PubMed Central - PubMed

Affiliation: Department of Physiology, Yanbian University School of Medicine, 977 Gongyuan Road, Yanji, Jilin 133002, China.

ABSTRACT
Our previous studies have shown that CNP-NPR-B/pGC-cGMP is upregulated in the diabetic rats. The present study was designed to determine whether the upregulation of CNP-NPR-B/pGC-cGMP signal pathway affects cGMP-PDE3-cAMP signal pathway in diabetic gastric smooth muscle. The gastric smooth muscle motility was observed by using isometric measurement. PDEs expressions in diabetic gastric smooth muscle tissue were observed by using immunohistochemistry, Western blotting, and RT-PCR methods. The results demonstrated that the inhibitory effect of CNP on the spontaneous contraction of gastric antral circular smooth muscle was potentiated in STZ-induced diabetic rat. CNP-induced increase of cGMP and cAMP was much higher in diabetic gastric smooth muscle tissue than in controls. The expression of PDE3 is downregulated while the levels of gene expression of PDE1, PDE2, PDE4, and PDE5 were not altered in the diabetic gastric smooth muscle tissue. The results suggest that the sensitivity of gastric smooth muscle to CNP is potentiated via activation of CNP-pGC-cGMP-PDE3-cAMP signal pathway in STZ-induced diabetic rats, which may be associated with diabetes-induced gastric motility disorder.

No MeSH data available.


Related in: MedlinePlus