Omeprazole suppresses endothelial calcium response and eNOS Ser1177 phosphorylation in porcine aortic endothelial cells

Kamiya, Chiaki; Odagiri, Keiichi; Hakamata, Akio; Sakurada, Ryugo; Inui, Naoki; Watanabe, Hiroshi

doi:10.1007/s11033-021-06561-0

Cited by 4 publications

(7 citation statements)

References 39 publications

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“…Endothelial cells constantly generate PGI2 and NO. Furthermore, Kamiya et al [ 55 ] also demonstrated that without BK or OME, the production rates of NO and PGI2 were 0.042 ± 0.032 µM/106 cells and 784.46 ± 212.45 pg/mL/106 cells, respectively, showing that both NO and PGI2 were produced at steady rates. For NO and PGI2, the effect of BK on these EDRF generation was increased by roughly 1.32 and 1.24 times, respectively, showing that the OME reduced the extra effect of BK on EDRF synthesis by roughly 0.96 times for NO and 1.03 times for PGI2.…”

Section: Discussionmentioning

confidence: 99%

Cardiotoxic Effects Produced by Omeprazole and Methylene Blue in an Animal Model of Cardiac Ischemia and Reperfusion and Potential Implications for the Pharmacological Strategy for Vasoplegic Syndrome

de Araújo,

Tallo,

Oliveira

et al. 2024

Biomedicines

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Defined as systemic hypotension caused by intense vasodilation due to the loss of systemic vascular resistance, vasoplegic syndrome (VS) is associated with elevated morbidity and mortality in humans. Although vasopressors such as norepinephrine and vasopressin are the first-choice drugs for VS treatment, several other drugs such as methylene blue (MB) can be used as adjuvant therapy including rescue therapy. To develop new pharmacological strategies to reduce the risk of VS, we investigated the effects of treatments with MB (2 mg/kg/IV), omeprazole (OME, 10 mg/kg/IV), and their combination in an animal model of cardiac ischemia–reperfusion (CIR). The ventricular arrhythmia (VA), atrioventricular block (AVB), and lethality (LET) incidence rates caused by CIR (evaluated via ECG) and serum levels of the cardiac lesion biomarkers creatine kinase–MB (CK-MB) and troponin I (TnI) in adult rats pretreated with saline solution 0.9% and submitted to CIR (SS + CIR group) were compared to those pretreated with MB (MB + CIR group), OME (OME + CIR group), or the MB + OME combination (MB + OME + CIR group). The AVB and LET incidence rates in the MB + CIR (100%), OME + CIR (100%), and MB + OME + CIR (100%) groups were significantly higher compared to the SS + CIR group (60%). The serum level of CK-MB in these groups were also significantly higher compared to the SS + CIR group, demonstrating that the treatments before CIR with MB, OME, and MB + OME produced similar effects in relation to cardiac function and the occurrence of lesions. These results demonstrate that the treatment of animals subjected to the CIR protocol with OME produced the same effects promoted by the treatment with MB, which may suggest the possibility of using OME alone or in combination with MB in medical clinics in treatment of VS.

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Section: Discussionmentioning

confidence: 99%

Cardiotoxic Effects Produced by Omeprazole and Methylene Blue in an Animal Model of Cardiac Ischemia and Reperfusion and Potential Implications for the Pharmacological Strategy for Vasoplegic Syndrome

de Araújo,

Tallo,

Oliveira

et al. 2024

Biomedicines

View full text Add to dashboard Cite

show abstract

“…In contrast, cardiovascular events are increased because of drug interactions between antiplatelet drugs and PPIs. [8][9][10] This phenomenon exists regardless of aspirin monotherapy, clopidogrel monotherapy, or dual antiplatelet therapy. [8][9][10] Patients treated with aspirin and PPIs had higher platelet aggregation, soluble serum P-selectin levels and serum thromboxane B2 levels, compared with patients not taking PPIs.…”

Section: Inhibition Of Antiplatelet Aggregation and Possible Counterm...mentioning

confidence: 99%

“…[8][9][10] This phenomenon exists regardless of aspirin monotherapy, clopidogrel monotherapy, or dual antiplatelet therapy. [8][9][10] Patients treated with aspirin and PPIs had higher platelet aggregation, soluble serum P-selectin levels and serum thromboxane B2 levels, compared with patients not taking PPIs. Thus, CHD patients treated with PPIs have a decreased platelet response to aspirin, as manifested by increased residual platelet aggregation and platelet activation.…”

Section: Inhibition Of Antiplatelet Aggregation and Possible Counterm...mentioning

confidence: 99%

“…[32][33][34][35] PPIs attenuate the antiplatelet aggregation of aspirin and clopidogrel. [8][9][10] Thus, when patients do not have to take PPIs, but need to take symptomatic drugs because of symptoms such as digestive tract discomfort, clinicians may consider using H2-receptor antagonists (H2RA) instead of PPIs. Cardiac H2 receptor activation may promote cardiac fibrosis and apoptosis.…”

Section: Inhibition Of Antiplatelet Aggregation and Possible Counterm...mentioning

confidence: 99%

“…[5][6][7] Long-term use of PPIs also leads to vascular endothelial dysfunction and endothelial senescence, and reduces the production of endothelium-derived diastolic factor EDRF. 8,9 There are some other side effects, including induction of hypomagnesemia, iron deficiency, vitamins D and K deficiency, etc. Ultimately, these side effects lead to an increase in cardiovascular events (Figure 1).…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Inappropriate Use of Proton Pump Inhibitors Increases Cardiovascular Events in Patients with Coronary Heart Disease

Hu¹,

Luo²,

Yang³

2022

IJGM

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Antiplatelet drugs, as the cornerstone of the treatment of coronary heart disease, control the progression of the disease, but bring a higher risk of gastrointestinal bleeding. Relevant guidelines recommend the use of proton pump inhibitors (PPIs) to minimize the risk of gastrointestinal bleeding in patients receiving dual antiplatelet therapy. But for people at low risk of gastrointestinal bleeding, the harms associated with routine use of PPIs may far outweigh the benefits. PPIs increase the risk of lower gastrointestinal bleeding, inhibit the effect of antiplatelet drugs, impair vascular endothelial function, meanwhile induce hypomagnesemia, iron deficiency, vitamins D and K deficiency, etc. Eventually, PPIs may lead to an increase in cardiovascular events. However, the situation is that PPIs are often overused. This review elucidates the mechanisms by which PPIs increase cardiovascular events, thereby reminding clinicians to rationally prescribe PPIs.

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Inhibitors of gastric acid secretion increase oxidative stress and matrix metalloproteinase-2 activity leading to vascular remodeling

Nogueira,

Sanches-lopes,

Oliveira-Paula

et al. 2024

Mol Cell Biochem

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Omeprazole suppresses endothelial calcium response and eNOS Ser1177 phosphorylation in porcine aortic endothelial cells

Cited by 4 publications

References 39 publications

Cardiotoxic Effects Produced by Omeprazole and Methylene Blue in an Animal Model of Cardiac Ischemia and Reperfusion and Potential Implications for the Pharmacological Strategy for Vasoplegic Syndrome

Cardiotoxic Effects Produced by Omeprazole and Methylene Blue in an Animal Model of Cardiac Ischemia and Reperfusion and Potential Implications for the Pharmacological Strategy for Vasoplegic Syndrome

Inappropriate Use of Proton Pump Inhibitors Increases Cardiovascular Events in Patients with Coronary Heart Disease

Inhibitors of gastric acid secretion increase oxidative stress and matrix metalloproteinase-2 activity leading to vascular remodeling

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