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5-dimethylamiloride

has anti-HIV-1 activity
Also Known As:
3-amino-5-dimethylamino-6-chloro-N-(diaminomethylene)pyrazinecarboxamide; 5-(N,N-dimethyl) amiloride; 5-(N,N-dimethyl)amiloride; 5-DMA; MK 685; MK-685; dimethyl amylioride; dimethylamiloride
Networked: 23 relevant articles (3 outcomes, 1 trials/studies)

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Bio-Agent Context: Research Results

Experts

1. Fujii, Nobutaka: 1 article (11/2012)
2. Fukuda, Yasunori: 1 article (11/2012)
3. Futaki, Shiroh: 1 article (11/2012)
4. Gräslund, Astrid: 1 article (11/2012)
5. Hatanaka, Yasumaru: 1 article (11/2012)
6. Kawaguchi, Yoshimasa: 1 article (11/2012)
7. Langel, Ulo: 1 article (11/2012)
8. Masuda, Ryo: 1 article (11/2012)
9. Matsuoka, Masao: 1 article (11/2012)
10. Nakase, Ikuhiko: 1 article (11/2012)

Related Diseases

1. Reperfusion Injury
2. Contracture
3. Ischemia
11/01/1997 - "To investigate whether an Na+/H+ exchange inhibitor would alter the reduced acidification during ischemia, we preconditioned hearts with and without dimethylamiloride (DMA). "
09/01/1996 - "The effects of 5-(N,N-dimethyl)amiloride, a potent and specific Na(+)-H+ exchange inhibitor, were investigated in isolated perfused rabbit hearts subjected to ischemia and reperfusion. "
05/01/2007 - "Selective inhibition of NHE-1 using dimethylamiloride significantly attenuated ischemia-induced infarct volume in hypertensive SHR following MCAO, suggesting a novel role for NHE-1 in the brain in the regulation of ischemia-induced infarct volume in SHR."
11/01/1997 - "To help resolve the controversy as to whether or not Na(+)-H+ exchange is functioning during reperfusion of the ischemic myocardium we assessed the effects of dimethylamiloride (DMA, an amiloride analogue possessing selectivity for inhibition of the Na(+)-H+ exchanger) on cardiac function and intracellular pH during ischemia-reperfusion. "
08/01/1989 - "The findings support the hypothesis that the effect of removing Na+ is mediated through a decrease in intracellular pH. These include observations that: (a) reducing internal pH by reducing external pH caused a decrease in gK1, and the conductance changes caused by reducing extracellular pH and removing extracellular Na+ were not additive: (b) the effect of reducing pHo was attenuated by dialyzing with a low pH internal solution; (c) gK1 was reduced by exposure to the Na-proton exchange inhibitor dimethylamiloride, and this effect was absent in the absence of Na+. These findings imply that physiological or pathological processes such as ischemia and metabolic or respiratory acidosis which can produce intracellular acidosis should be expected to affect K+ permeation through the IK1 channel."
4. Acidosis
05/01/1994 - "The administration of dimethylamiloride completely prevented both the mechanical and energetic disorders after correction of acidosis. "
05/01/1994 - "To examine this hypothesis, dimethylamiloride, a selective Na(+)-H+ exchange inhibitor, was administered just before the correction of acidosis in the other seven hearts. "
01/01/1989 - "The Na+-K+ pump-induced hyperpolarization was abolished (Emax = -22.6 +/- 1.6 mV, n = 8, P less than 0.001) by 10 microM 5-(N,N-dimethyl)amiloride and, when the extracellular Na+ concentration was reduced to 50 mM, by 50 mM Li+. These findings suggest that Na+-H+ exchange can produce a Na+ load which then can stimulate electrogenic Na+ pumping in human cardiac cells during recovery from acidosis."
01/20/2003 - "Dimethylamiloride (DMA) (10 microM) abolished activation of the Rb(+)/K(+) efflux in the second model; however, Na(+)/H(+) exchanger was not involved, because intracellular acidosis induced by the hyposmotic shock was not enhanced by DMA treatment. "
08/01/1989 - "The findings support the hypothesis that the effect of removing Na+ is mediated through a decrease in intracellular pH. These include observations that: (a) reducing internal pH by reducing external pH caused a decrease in gK1, and the conductance changes caused by reducing extracellular pH and removing extracellular Na+ were not additive: (b) the effect of reducing pHo was attenuated by dialyzing with a low pH internal solution; (c) gK1 was reduced by exposure to the Na-proton exchange inhibitor dimethylamiloride, and this effect was absent in the absence of Na+. These findings imply that physiological or pathological processes such as ischemia and metabolic or respiratory acidosis which can produce intracellular acidosis should be expected to affect K+ permeation through the IK1 channel."
5. Infarction (Infarctions)

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4. Amiloride (Midamor)
5. Sodium-Hydrogen Exchangers
6. Calcium
7. Protons (Proton)
8. Vacuolar Proton-Translocating ATPases (V-Type ATPase)
9. Sodium-Calcium Exchanger
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