Isoform-specific regulation of the Na+-K+ pump by adenosine in guinea pig ventricular myocytes

Zhang, Zhe; Guo, Huicai; Zhang, Linan; Wang, Yongli

doi:10.1038/aps.2009.26

Cited by 5 publications

(5 citation statements)

References 30 publications

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“…4 The A 3– selective agonist Cl-IB-MECA was able to induce protection against hypoxia in a neonatal rat cardiomyocyte model, 35 but there are little available data confirming whether A 3 AR are actually expressed in adult cardiac myocytes. Zhang et al 36 found that A 1 AR-selective agonists inhibited high dihydro-ouabain sensitive Na + -K + current in guinea pig ventricular myocytes, whereas Cl-IB-MECA had no effect causing them to conclude that adult cardiomyocytes do not express A 3 AR, at least in that species. The present results, however, clearly reveal A 3 AR in the sarcolemma of adult rabbit cardiomyocytes.…”

Section: Discussionmentioning

confidence: 99%

All Preconditioning-Related G Protein-Coupled Receptors Can Be Demonstrated in the Rabbit Cardiomyocyte

Xin

Yang

Rich

et al. 2011

J Cardiovasc Pharmacol Ther

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G protein-coupled receptors for adenosine (A1, A3, A2A and A2B), bradykinin (B1) and opioids (δ) are all involved in the mechanism of ischemic preconditioning. Although the heart is comprised of many tissue types it has been assumed that preconditioning’s protective signaling occurs in the cardiomyocyte. We critically tested that hypothesis by testing for the presence of each of these receptors in isolated adult rabbit ventricular myocytes that had been transfected with cyclic nucleotide-gated (CNG) ion channels. Because subsarcolemmal cAMP opens the CNG channels we could monitor cAMP levels within a single cardiomyocyte by measuring channel current with a patch pipette. The presence of a receptor would be confirmed if we could alter cAMP in the cell with a selective agonist to the receptor being studied. Superfusion with the β-adrenergic Gs-coupled receptor agonist isoproterenol (50 nM) transiently increased cAMP levels, and, therefore, channel current. Pretreatment with selective agonists to A1 or A3 adenosine receptors (AR) that are Gi-coupled markedly attenuated the response to isoproterenol indicating inhibition of adenylyl cyclase by increased Gi activity. Agonists to bradykinin or δ-opioid receptors also attenuated isoproterenol’s response. A2AAR and A2BAR are Gs-coupled. The A2AAR–selective agonist CGS21680 increased current through CNG channels but only in the presence of phosphodiesterase (PDE) inhibitors indicating low surface receptor activity and high intracellular PDE activity. As we previously reported, BAY 60–6583, an A2BAR-selective agonist which mimics preconditioning’s protection in rabbit heart, neither increased nor decreased membrane current in transfected cardiomyocytes, suggesting absence or a markedly limited number of A2BAR in the sarcolemma. However, RT-PCR of purified cardiomyocytes yielded an A2BAR band implying that rabbit cardiomyocytes do indeed express A2BAR. These data reveal that all receptors reported to be involved in ischemic preconditioning do exist on or within the cardiomyocyte.

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Section: Discussionmentioning

confidence: 99%

All Preconditioning-Related G Protein-Coupled Receptors Can Be Demonstrated in the Rabbit Cardiomyocyte

Xin

Yang

Rich

et al. 2011

J Cardiovasc Pharmacol Ther

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“… 22) Interestingly, some researchers reported that artemisinin has an antiarrhythmic effect by inhibiting multiple ion channels. 9) 10) Yang et al 7) 8) demonstrated that artemisinin significantly inhibited the potassium outward current of I to channels in the Purkinje fibers by 84% at 100 μM in a concentration-dependent and reversible manner. The concentration of artemisinin used (100–150 μM) in the current study was based on that report.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to its antimalarial effect, its antiarrhythmic effect, which includes suppression of the I K1 , I to , and I Ks channels, was reported previously. 7) 8) 9) 10) Therefore, we evaluated the hypothesis that inhibition of I to channels by artemisinin may play a role in the suppression of ventricular arrhythmia in canine wedge preparation models of BrS.…”

Section: Introductionmentioning

confidence: 99%

Antiarrhythmic Effect of Artemisinin in an Ex-vivo Model of Brugada Syndrome Induced by NS5806

et al. 2023

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Author's summary According to current guidelines, an implantable cardioverter-defibrillator (ICD) is the first-line therapy for Brugada syndrome. But, fundamentally, ICD is not a therapeutic modality. We have quinidine. However, it has several adverse effects. The present study shows that artemisinin suppresses the development of ventricular tachyarrhythmia by inhibition of I to channels. The safety of artemisinin was verified in malarial treatment. Therefore, it is meaningful as a drug re-position and there might be a possibility to use for Brugada syndrome in real-world practice if the efficacy is verified in following clinical studies.

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“…The postulated mechanisms include 1) These were in the distribution area of the facial nerve, and the volume of bee venom was large. Melittin might inhibit the activity of Na + -K + -ATPase on the nerve synapse through the above mechanism, 12 resulting in facial nerve paralysis. 2) Bee venom is composed of proteins like hyaluronidase, phospholipase, peptides like secapin, apamin, procamine, and active amines like histamine and apamin.…”

Section: Discussionmentioning

confidence: 99%

Analysis of a Case of Facial Nerve Injury Caused by Bee Sting in a Child

Li¹,

Xiang²,

Lv³

2023

RMHP

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Background: Bee sting injuries in children are accidental and occur in rural areas in summer and autumn. They have the characteristics of rapid onset, rapid change, many complications, complex treatment, and high disability rate. Patients experience various symptoms, such as vomiting, diarrhea, dyspnea, angioedema, multiple neuritis, myocardial infarction, acute renal failure, hypotension, and collapse. Systemic complications of the nervous system are rare. However, some cases of stroke, optic neuritis, and acute disseminated encephalomyelitis are related to bee stings. There are many cases of systemic multiple organ dysfunctions after bee sting injury, but there are few reports of facial nerve injury. The case presented here was caused by bee venom. This report is important because there are few instances of facial paralysis in the large number of notified bee sting cases. After active treatment, the facial paralysis of the child recovered gradually. Case Presentation: The patient was a 6-year-old boy. The bee stings by bee swarm induced pain in many parts of the body for 8 h. After the injury, he had skin itching, rash, swelling, and pain in the head and face. The boy had soy sauce-colored urine later and was transferred to the Affiliated Hospital of Zunyi Medical University from a lower-level hospital for treatment. On the seventh day after transfer, the child suddenly suffered from deviated mouth, which was considered a delayed facial nerve injury. After active treatment, he recovered from facial paralysis and was discharged from the hospital. Conclusion: This case report adds the clinical manifestation of facial paralysis after bee stings. They require close observation and being alert to possible clinical manifestations, as well as carrying out active intervention treatment.

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Isoform-specific regulation of the Na+-K+ pump by adenosine in guinea pig ventricular myocytes

Cited by 5 publications

References 30 publications

All Preconditioning-Related G Protein-Coupled Receptors Can Be Demonstrated in the Rabbit Cardiomyocyte

All Preconditioning-Related G Protein-Coupled Receptors Can Be Demonstrated in the Rabbit Cardiomyocyte

Antiarrhythmic Effect of Artemisinin in an Ex-vivo Model of Brugada Syndrome Induced by NS5806

Analysis of a Case of Facial Nerve Injury Caused by Bee Sting in a Child

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