Publications by authors named "K Ayajiki"

Article Synopsis
  • * A retrospective analysis on cardiovascular outpatients indicates that lower kidney function and higher white blood cell counts are linked to NLR elevation, while animal experiments suggest changes in bone marrow processes are involved.
  • * Findings reveal that renal impairment significantly affects NLR through alterations in hematopoiesis, with indoxyl sulfate (IS) playing a key role; treatment with an adsorbent normalizes NLR and bone marrow changes in mice.
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Article Synopsis
  • Vasodilators like prostacyclin, nitric oxide (NO), and endothelium-derived hyperpolarizing factor (EDHF) play a critical role in regulating systemic blood pressure.
  • This study examines how NO interacts with EDHF during acetylcholine and bradykinin-induced blood pressure responses in anesthetized rats, identifying specific potassium channels involved in this process.
  • Findings suggest that endothelial hyperpolarization and gap junctions, rather than diffusible substances, are key in mediating the depressor responses, with NO potentially dampening the effects of EDHF through increased cGMP levels.
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Excitation of the renal sympathetic nervous system is important for the development of ischaemic acute kidney injury (AKI) in rats. We reported that intravenous treatment with GABA has preventive effects against ischaemia/reperfusion (I/R)-induced renal dysfunction with histological damage in rats; however, the mechanisms underlying these effects on renal injury remain unknown. Thus, the aim of the present study was to clarify how GABA mechanistically affects ischaemic AKI in rats.

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Increasing evidence supports the idea that chronic hypoperfusion in the brain is responsible for the pathogenesis underling Alzheimer's disease (AD). Obesity at midlife is associated with the risk of cognitive loss and AD at later life. Obesity decreases cerebral blood flow that is associated with decreased synthesis and actions of nitric oxide (NO) derived from the endothelium and also increases the production of oxidative stress.

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Time-dependent changes in the renal sympathetic nerve activity (RSNA) in the progression of chronic kidney disease (CKD) have not been investigated, despite the fact that renal sympathetic nervous system is augmented in the condition of CKD. In the present study, we examined time-dependent changes in RSNA and renal venous norepinephrine concentrations for 12 weeks using 5 of 6 nephrectomized CKD rats. Both RSNA and norepinephrine concentrations were increased during the early phase in the progression of CKD.

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