κ-Opioid receptor stimulation increases the expression of NA+-H+ exchange gene in the heart

Gan, Tracey X.; Pei, Jianming; Chan, Ivan; Wong, Tak‐Ming

doi:10.1016/s0024-3205(99)00597-4

Cited by 5 publications

(4 citation statements)

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“…14,15) In addition, angiotensin II and kappa-opioid receptor stimulation regulate myocardial NHE1 in the in vivo rat heart. 3, 16,17) Thus, the regulation of NHE1 in non-infarcted myocardium may be partially mediated by neurohumoral factors, such as the renin-angiotensin system. On the other hand, NHE1 is regulated in response to a variety of extracellular stimuli, not only agonists such as growth factors and hormones, but also mechanical stimuli such as osmotic stress and cell spreading.…”

Section: )mentioning

confidence: 99%

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

et al. 2002

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SUMMARYAlthough cardiac NHE1 is activated during myocardial ischemia and reperfusion injury, little is known about changes in expression in non-infarcted myocardium after acute myocardial infarction (AMI). The purpose of this study was to examine left ventricular function and region dependent NHE1 expression after myocardial infarction. Therefore, we produced two AMI models in rats, a small infarction model which was continuously ligated at the branches of the left coronary artery, and an extensive infarction model continuously ligated at the root of the artery. We examined NHE1 mRNA expression using RNase protection assay and protein levels using Western blot analysis in noninfarcted myocardium during the 24 hour period after AMI. The level of NHE1 mRNA and protein expression in the whole heart including the infarcted myocardium did not change after a small infarction. On the other hand, in the case of an extensive infarction, the levels of NHE1 mRNA and protein expression decreased significantly by 21.5% (P<0.05) and by 22.0% (P<0.05), respectively, in non-infarcted myocardium. Left ventricular systolic pressure (LVSP) decreased significantly by 13% and 38% with the branch and root ligation, respectively. However, left ventricular end-diastolic pressure (LVEDP) only increased with the root ligation. These results indicate that NHE1 expression decreased in response to extensive myocardial infarction only in non-infarcted myocardium. The present study may be important in furthering the understanding of NHE1 in myocardial infarction and suggests that decreased expression of NHE1 in non-infarcted myocardium may decrease the extent of cardiac cell injury. (Jpn Heart J 2002; 43: 273-282)

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confidence: 99%

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

et al. 2002

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“…Ca 2+ ‐calmodulin and protein kinase C are involved in the regulation of the H + /K + ‐ATPase in rat distal colon (Heinke et al. 1999) and these signals are also involved in regulation of the Na + /H + exchanger 1 (NHE1) in rat ventricular myocytes (Gan et al. 2000, Fliegel 2001).…”

Section: Discussionmentioning

confidence: 99%

“…Renal tubular H + /K + -ATPase is strongly stimulated by K + depletion (Garg & Narang 1990, Silver & Soleimani 1999. Ca 2+calmodulin and protein kinase C are involved in the regulation of the H + /K + -ATPase in rat distal colon (Heinke et al 1999) and these signals are also involved in regulation of the Na + /H + exchanger 1 (NHE1) in rat ventricular myocytes (Gan et al 2000, Fliegel 2001). These observations suggest that the H + /K + -ATPase in heart may also be regulated through Ca 2+ -calmodulin and PKC pathways, and that the H + /K + -ATPase may be partly responsible for the regulation of pH i in the cardiac myocytes.…”

Section: Discussionmentioning

confidence: 99%

Identification and regulation of the gastric H⁺/K⁺‐ATPase in the rat heart

Beisvåg

Falck

Loennechen

et al. 2003

Acta Physiologica Scandinavica

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“…This, in turn, contributes to the increase in [Ca 2ϩ ] i via Na ϩ -Ca 2ϩ exchange. Na ϩ -H ϩ -exchange gene expression in the heart is increased upon -opioid receptor stimulation (34). Another explanation for the increased [Ca 2ϩ ] i is the decreased Ca 2ϩ uptake into the sarcoplasmatic reticulum upon protein kinase C activation.…”

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confidence: 99%

??-Opioid Receptor Antagonism Improves Recovery from Myocardial Stunning in Chronically Instrumented Dogs

Hartlage¹,

Theisen²,

Oliveira³

et al. 2006

Anesthesia & Analgesia

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We tested the hypothesis that the selective kappa-opioid receptor antagonist nor-binaltorphimine (nor-BNI) improves recovery from myocardial stunning. Ten dogs were chronically instrumented for measurement of heart rate, left atrial, aortic and left ventricular pressure (LVP), and the maximum rate of LVP increase (LV dP/dt(max)) and decrease (LV dP/dt(max)), coronary blood flow velocity and myocardial wall-thickening fraction. Regional myocardial blood flow was determined with fluorescent microspheres. Catecholamine plasma levels were measured by high-performance liquid chromatography, and beta-endorphin and dynorphin plasma levels by radioimmunoassay. An occluder around the left anterior descending artery (LAD) allowed induction of a reversible LAD-ischemia. Animals underwent two experiments in a randomized crossover fashion on separate days: (a) 10 min LAD-occlusion (control experiment), (b) second ischemic episode 24 h after nor-BNI (2.5 mg/kg IV) (intervention). Dogs receiving nor-BNI showed an increase in wall-thickening fraction, LV dP/dt(max) and LV dP/dt(min) before ischemia and during the whole reperfusion (P < 0.05 versus control experiment). After nor-BNI pretreatment, dynorphin levels increased after induction of ischemia to a peak level of 15.1 +/- 3.6 pg/mL (P < 0.05 versus control experiment). The increase in plasma beta-endorphin during ischemia and early reperfusion was attenuated after nor-BNI. Compared with the control experiment, nor-BNI left global hemodynamics, regional myocardial blood flow, and catecholamine levels unchanged. In conclusion, nor-BNI improves recovery from myocardial stunning after regional myocardial ischemia in chronically instrumented dogs.

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κ-Opioid receptor stimulation increases the expression of NA+-H+ exchange gene in the heart

Cited by 5 publications

References 20 publications

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

Identification and regulation of the gastric H⁺/K⁺‐ATPase in the rat heart

??-Opioid Receptor Antagonism Improves Recovery from Myocardial Stunning in Chronically Instrumented Dogs

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κ-Opioid receptor stimulation increases the expression of NA+-H+ exchange gene in the heart

Cited by 5 publications

References 20 publications

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

Decreased Expression of Na+/H+ Exchanger Isoform 1 (NHE1) in Non-infarcted Myocardium after Acute Myocardial Infarction.

Identification and regulation of the gastric H+/K+‐ATPase in the rat heart

??-Opioid Receptor Antagonism Improves Recovery from Myocardial Stunning in Chronically Instrumented Dogs

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Identification and regulation of the gastric H⁺/K⁺‐ATPase in the rat heart