Natriuretic peptides cause relaxation of human and guinea-pig gallbladder muscle through interaction with natriuretic peptide receptor-B

Lee, Ming-Che; Hu, Huai-Chin; Huang, Shih-Che

doi:10.1016/j.regpep.2005.01.006

Cited by 7 publications

(14 citation statements)

References 23 publications

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“…CNP was found to be released from endothelial cells of the perfused rat mesenteric bed in response to endotheliumdependent vasodilators such as acetylcholine (5,6). CNP induced hyperpolarization and relaxation of mesenteric artery vascular smooth muscle through activation of natriuretic peptide receptor subtype B and the same potassium channels that are activated by EDHF (5)(6)(7)(8). In this study, we provide evidence that epineurial arterioles of the sciatic nerve contain CNP, predominantly in endothelial cells, and that exogenous CNP causes vascular relaxation that can be prevented by potassium channel blockers that we have previously shown inhibit the EDHF component of acetylcholine-mediated vascular relaxation (9).…”

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confidence: 99%

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Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

et al. 2007

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In epineurial arterioles, acetylcholine-mediated vascular relaxation is mediated by nitric oxide and endotheliumderived hyperpolarizing factor (EDHF), and both mechanisms are impaired by diabetes. The mediator responsible for the effect of EDHF is unknown. In epineurial arterioles, C-type natriuretic peptide (CNP) has properties consistent with EDHF-like activity. Epineurial arterioles express CNP, and exogenous CNP causes a concentration-dependent vascular relaxation. In streptozotocin-induced diabetic rats, CNP-mediated vascular relaxation in epineurial arterioles is decreased. Since CNP may be a regulator of vascular function, a vasopeptidase inhibitor may be an effective treatment for diabetes-induced vascular and neural disease. Vasopeptidase inhibitors inhibit ACE activity and neutral endopeptidase, which degrades natriuretic peptides. Streptozotocin-induced diabetic rats were treated with AVE7688 (450 mg/kg in the diet), a vasopeptidase inhibitor, for 8 -10 weeks after 4 weeks of untreated diabetes. Treatment of diabetic rats corrected the diabetesinduced decrease in endoneurial blood flow, significantly improved motor and sensory nerve conduction velocity, prevented the development of hypoalgesia in the hind paw, and reduced superoxide and nitrotyrosine levels in epineurial arterioles. The diabetes-induced decrease in acetylcholine-mediated vascular relaxation by epineurial arterioles was significantly improved with treatment. These studies suggest that vasopeptidase inhibitors may be an effective approach for the treatment of diabetic vascular and neural dysfunction. Diabetes 56:355-362, 2007 S tudies performed in our laboratory with streptozotocin-induced diabetic rats have provided evidence that the generation of oxidative stress through the production of superoxide and peroxynitrite impairs vascular function of epineurial arterioles of the sciatic nerve, and this precedes slowing of motor nerve conduction velocity (MNCV) (1-3). These studies imply that hyperglycemia-induced oxidative stress may be responsible for diabetes-induced vascular and neural dysfunction that occurs during diabetic neuropathy.We have recently reported that the ACE inhibitor Enalapril was an effective treatment for vascular and neural disease in streptozotocin-induced diabetic rats (4). These results and our studies with C-type natriuretic peptide (CNP), demonstrating its vascular relaxation properties in epineurial arterioles, provide rationale to test the effect of vasopeptidase inhibitors on diabetic neuropathy.It has been reported in mesenteric resistance arteries that release of CNP accounts for the biological activity of endothelium-derived hyperpolarizing factor (EDHF) (5,6). CNP was found to be released from endothelial cells of the perfused rat mesenteric bed in response to endotheliumdependent vasodilators such as acetylcholine (5,6). CNP induced hyperpolarization and relaxation of mesenteric artery vascular smooth muscle through activation of natriuretic peptide receptor subtype B and the same potassium channels that...

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confidence: 99%

“…The bioactive form of CNP is a 22-amino acid peptide. Like ANP and BNP, CNP is expressed and stored as a prohormone and converted to the active peptide by a multistep process involving a ubiquitous proprotein convertase called furin (8,11).…”

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Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

et al. 2007

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“…Measurements of contraction and relaxation of muscle strips from the human gallbladder were performed according to procedures described previously [1819]. In brief, human gallbladder muscle strips (1.0 cm × 0.3 cm) were suspended in organ baths and incubated at 37°C in standard incubation solution (118mM NaCl, 25mM NaHCO 3 , 4.7mM KCl, 14mM glucose, 1.2mM NaH 2 PO 4 , 1.8mM CaCl 2 , pH 7.4) gassed with 95% O 2 –5% CO 2 .…”

Section: Methodsmentioning

confidence: 99%

Estrogen and G protein-coupled estrogen receptor agonist G-1 cause relaxation of human gallbladder

Lee

Yang

Chen

et al. 2016

Tzu Chi Medical Journal

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Objective:Estrogen interacts with a membrane receptor, G protein-coupled estrogen receptor (GPER). It was reported that 17β-estradiol was able to inhibit contraction of the human colon and cause relaxation of the guinea pig gallbladder, however, the involvement of GPER was not clarified. The aim of the present study was to investigate the effect of estrogen on human gallbladder motility and the possible role of GPER.Materials and Methods:Relaxation of human gallbladder strips were measured using isometric transducers. Expression of GPER was evaluated by reverse transcription polymerase chain reaction (PCR), realtime PCR, and immunohistochemistry.Results:In human gallbladder strips, 17β-estradiol and G-1 elicited marked and rapid relaxation, whereas tamoxifen produced mild concentration-dependent relaxation. The relative efficacies to cause relaxation were as follows: 17β-estradiol = G-1 > tamoxifen. The relaxant response of 17β-estradiol was not attenuated by tetrodotoxin or conotoxin GVIA. This implies that nerve stimulation was not involved in the 17β-estradiol-induced gallbladder relaxation. Analysis by reverse transcription PCR and real-time PCR showed that GPER was expressed in the human gallbladder. Further analysis by immunohisto-chemistry revealed that GPER was expressed in the gallbladder muscle. This suggests that 17β-estradiol relaxes the human gallbladder via GPER.Conclusion:These results demonstrate for the first time that 17β-estradiol and GPER agonist G-1 cause relaxation of the human gallbladder, probably through GPER. Estrogen might play an important role in the control of human gallbladder motility.

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“…In addition, ANP and CNP inhibit contraction in the stomach [10,15] whereas ANP, BNP, CNP, and DNP inhibit contraction in the colon and cecum [8,10,16e18]. In the biliary system, CNP elicits relaxation in the gallbladder [19]. NPRs have been identified in various gastrointestinal tissues.…”

Section: Introductionmentioning

confidence: 99%

“…Natriuretic peptides stimulate relaxation of gastrointestinal smooth muscle through NPR-A, NPR-B, or NPR-C. NPR-A mediates relaxation of the lower esophageal sphincter [14]. NPR-B promotes relaxation of the esophagus and gallbladder, whereas NPR-C mediates relaxation of the stomach [12,16,19]. ANP has been reported to cause relaxation in the internal anal sphincter (IAS) [13].…”

Section: Introductionmentioning

confidence: 99%

C-type atriuretic peptide causes relaxation of the internal anal sphincter through natriuretic peptide receptor B

Huang

2015

Tzu Chi Medical Journal

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a b s t r a c tObjectives: The internal anal sphincter (IAS) plays an important role in maintaining continence. Atrial natriuretic peptide (ANP) could relax the IAS. The purpose of the present study was to investigate the roles of natriuretic peptide receptors (NPRs) in the IAS. Materials and methods: Relaxation of isolated rat IAS strips caused by natriuretic peptides was measured using isometric transducers. Expression of NPRs was evaluated by reverse transcriptionepolymerase chain reaction (PCR), immunohistochemistry and real-time PCR. Results: In the rat IAS, C-type natriuretic peptide (CNP) produced a marked and concentrationdependent relaxation while ANP caused a mild relaxation. By contrast, brain natriuretic peptide, dendroaspis natriuretic peptide, and des[Gln18, Ser19, Gly20, Leu21, Gly22]ANP(4e23) amide did not generate relaxation. CNP was much more effective than ANP and brain natriuretic peptide in stimulating the relaxation, indicating that NPR-B mediates IAS relaxation. The CNP-induced relaxation was inhibited by the protein kinase G inhibitor Rp-8CPT-cGMPS and potassium channel blocker charybdotoxin but not by protein kinase A inhibitor Rp-cAMPS. This suggests the involvement of cGMP and calcium-activated potassium channels in the CNP-induced IAS relaxation. Reverse transcription PCR and immunohistochemistry revealed the existence of NPR-B in the rat IAS. Furthermore, real-time PCR identified abundant expression of CNP and NPR-B in the rat IAS. Conclusion: CNP causes relaxation of the IAS via NPR-B, cGMP, and potassium channel pathways in rats. CNP might regulate IAS motility. NPR-B is a potential therapeutic target in anorectal motility disorders.

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Natriuretic peptides cause relaxation of human and guinea-pig gallbladder muscle through interaction with natriuretic peptide receptor-B

Cited by 7 publications

References 23 publications

Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

Treatment of Streptozotocin-Induced Diabetic Rats With AVE7688, a Vasopeptidase Inhibitor

Estrogen and G protein-coupled estrogen receptor agonist G-1 cause relaxation of human gallbladder

C-type atriuretic peptide causes relaxation of the internal anal sphincter through natriuretic peptide receptor B

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