The role of Na+/H+ exchanger in Ca2+ overload and ischemic myocardial damage in hearts from type 2 diabetic db/db mice

Anzawa, Ryuko; Seki, Shuichi; Nagoshi, Tomohisa; Taniguchi, Ikuo; Feuvray, D.; Yoshimura, Michihiro

doi:10.1186/1475-2840-11-33

Cited by 22 publications

(15 citation statements)

References 40 publications

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“…Although insulin is one of the NHE activators [22,23], diabetic condition (namely, hyperinsulinemia) as indicated by increased HbA1c, rather reduces ΔK. It is possible that other factors, such as intracellular acidification and some neurohumoral regulators, including the renin-angiotensin-aldosterone system are directly involved in the activation of NHE under the presence of insulin resistance [24,25].…”

Section: Discussionmentioning

confidence: 99%

Transient decrease in serum potassium level during ischemic attack of acute coronary syndrome: Paradoxical contribution of plasma glucose level and glycohemoglobin

Sekiyama

Nagoshi

Komukai

et al. 2013

Cardiovasc Diabetol

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BackgroundAlthough a decrease in serum potassium level has been suggested to be a fairly common observation in acute coronary syndrome (ACS), there have so far been no definitive reports directly demonstrating the transient potassium decrease (the potassium dip) during ischemic attack of ACS compared to stable phase in individual patients. To understand the pathophysiological significance of the potassium dip, we examined the changes in serum potassium level throughout ischemic attack and evaluated the clinical factors affecting it.MethodsThe degree of the potassium dip during ischemic attack (as indicated by ΔK, ΔK = K at discharge − K on admission) was examined in 311 consecutive patients with ACS who required urgent hospitalization in our institution.ResultsSerum potassium level during ischemic attack was significantly decreased compared to that during stable phase (P < 0.001). Multiple regression analysis revealed that plasma glucose level during attack was the sole factor which was positively correlated with ΔK (P < 0.01), while HbA1c level was negatively correlated (P < 0.05). The medication profiles and renal function had no impact on ΔK. A longer hospitalization period, higher incidence of myocardial infarction and higher peak creatine kinase level were observed in patients with a larger ΔK.ConclusionsWe have clearly demonstrated that there is a transient decrease in serum potassium level during ischemic attack of ACS compared to stable phase. The degree of the potassium dip was tightly correlated with glucose level, which overwhelmed the diabetic condition, and it also indicates the disease severity. The present study therefore promotes awareness of the significance of monitoring potassium level in parallel with glucose level in patients with ACS.

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Section: Discussionmentioning

confidence: 99%

Transient decrease in serum potassium level during ischemic attack of acute coronary syndrome: Paradoxical contribution of plasma glucose level and glycohemoglobin

Sekiyama

Nagoshi

Komukai

et al. 2013

Cardiovasc Diabetol

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“…Na + /H + exchange is pharmacologically inhibitable by NHE1-selective acylguanidine-derived compounds such as cariporide (HOE-642) [39,41,42]. Cariporide blunts the phosphorylation of NHE1 [31] and has been widely used to study putative functions of NHE1 in vitro and in vivo [24,41,43,44]. The influence of MG on NHE1 expression and functions remains elusive.…”

Section: Introductionmentioning

confidence: 99%

Endothelial Na + /H + exchanger NHE1 participates in redox-sensitive leukocyte recruitment triggered by methylglyoxal

Qadri

Shao‐Horn

Cayabyab

et al. 2014

Cardiovasc Diabetol

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Background: Excessive levels of methylglyoxal (MG) encountered in diabetes foster enhanced leukocyte-endothelial cell interactions, mechanisms of which are incompletely understood. MG genomically upregulates endothelial serum-and glucocorticoid-inducible kinase 1 (SGK1) which orchestrates leukocyte recruitment by regulating the activation and expression of transcription factors and adhesion molecules. SGK1 regulates a myriad of ion channels and carriers including the Na

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“…In some patients, heart failure is a result of segmental ischaemic injury caused by occlusive large vessel coronary artery disease; most (but not all) of these patients have a prior history of myocardial infarction. In others, heart failure presents with a reduced ejection fraction and global hypokinesis in the absence of large vessel coronary artery disease; the progressive and diffuse loss of cardiomyocytes may be related to diabetes‐related activation of the sodium‐hydrogen exchanger‐1 or Ca ++ /calmodulin‐dependent kinase II, the two most important mechanisms for programmed cell death …”

Section: Heart Failure Phenotypes In Patients With Type 2 Diabetesmentioning

confidence: 99%

Critical role of the epicardium in mediating cardiac inflammation and fibrosis in patients with type 2 diabetes

Packer

2019

Diabetes Obesity Metabolism

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The role of Na+/H+ exchanger in Ca2+ overload and ischemic myocardial damage in hearts from type 2 diabetic db/db mice

Abstract: Background: A higher increase in intracellular Na + via Na

Cited by 22 publications

References 40 publications

Transient decrease in serum potassium level during ischemic attack of acute coronary syndrome: Paradoxical contribution of plasma glucose level and glycohemoglobin

Transient decrease in serum potassium level during ischemic attack of acute coronary syndrome: Paradoxical contribution of plasma glucose level and glycohemoglobin

Endothelial Na + /H + exchanger NHE1 participates in redox-sensitive leukocyte recruitment triggered by methylglyoxal

Critical role of the epicardium in mediating cardiac inflammation and fibrosis in patients with type 2 diabetes

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