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Chemical Compound Review

SureCN7904048     2-amino-N-(2,6- dimethylphenyl)-N-(3...

Synonyms: Ro-22-9194, AC1L2V70, Tox21_113250, Ro 22-9194, 106134-33-2, ...
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Disease relevance of 2-amino-N-(2,6-dimethylphenyl)-N-(3-pyridin-3-ylpropyl)propanamide

 

High impact information on 2-amino-N-(2,6-dimethylphenyl)-N-(3-pyridin-3-ylpropyl)propanamide

  • Furthermore, Ro 22-9194 (30 mg/kg) attenuated the increase in venous thromboxane B2 concentrations in the local coronary vein during coronary ligation in dogs [1].
  • 6. Ro 22-9194 > or = 30 microM caused a slight decrease of calcium inward current (ICa) of myocytes without affecting the delayed rectifier potassium current (IK).(ABSTRACT TRUNCATED AT 250 WORDS)[2]
  • 5. In myocytes treated with Ro 22-9194 (30 microM), a 10 ms conditioning clamp to 0 mV caused a significant decrease in Vmax of the subsequent test action potential; further prolongation of the clamp pulse duration resulted in a modest enhancement of the Vmax inhibition [2].
  • These findings suggest that Ro 22-9194 more strongly inhibited the Na+ channel of the atrial myocytes of the diseased hearts with the depolarized membranes potentials than the Na+ channels in ventricular myocytes [3].
  • 3. The course of recovery from the use-dependent block, which was not affected by the membrane potential, was 4.0 sec, suggesting that Ro 22-9194 belongs to the intermediate kinetic class I drugs and it probably acts via a hydrophobic pathway [4].
 

Biological context of 2-amino-N-(2,6-dimethylphenyl)-N-(3-pyridin-3-ylpropyl)propanamide

 

Anatomical context of 2-amino-N-(2,6-dimethylphenyl)-N-(3-pyridin-3-ylpropyl)propanamide

  • Direct administration of Ro 22-9194 (1-300 micrograms) into the sinus node artery of the isolated atrium induced negative chrono- and inotropic responses and a transient increase in coronary blood flow in a dose-related manner [5].
  • Influence of extracellular H+ and Ca2+ on Ro 22-9194-induced block of sodium current in cardiac myocytes [6].

References

  1. Effects of the new class I antiarrhythmic agent Ro 22-9194, (2R)-2-amino-N-(2,6-dimethylphenyl)-N-[3-(3-pyridyl)propyl]propionamide D-tartrate, on ischemia- and reperfusion-induced arrhythmias in dogs: involvement of thromboxane A2 synthase inhibitory activity. Murakami, M., Kinukawa, M., Kanazawa, T., Maruyama, K., Miyagi, M., Miyata, H., Ujiie, A. J. Pharmacol. Exp. Ther. (1996) [Pubmed]
  2. Electrophysiological effects of Ro 22-9194, a new antiarrhythmic agent, on guinea-pig ventricular cells. Maruyama, K., Kodama, I., Anno, T., Suzuki, R., Toyama, J. Br. J. Pharmacol. (1995) [Pubmed]
  3. Tonic block of the Na+ current in single atrial and ventricular guinea-pig myocytes, by a new antiarrhythmic drug, Ro 22-9194. Hiroe, K., Hisatome, I., Tanaka, Y., Ahmmed, G.U., Sasaki, N., Shimoyama, M., Tsuboi, M., Inoue, Y., Manabe, I., Yamamoto, Y., Ohtahata, A., Kinugawa, T., Ogino, K., Igawa, O., Yoshida, A., Shigemasa, C., Sato, R. Fundamental & clinical pharmacology. (1997) [Pubmed]
  4. The blocking mechanism of sodium currents by a new class I antiarrhythmic drug, Ro 22-9194, in isolated guinea-pig ventricular myocytes. Karasaki, S., Sato, R., Katori, R. Gen. Pharmacol. (1997) [Pubmed]
  5. Cardiovascular effects of 2-amino-N-(2,6-dimethylphenyl)-N-[3-(3-pyridyl)propyl]propionamide dihydrochloride (Ro 22-9194) in the isolated, cross-perfused atrium of the dog. Murakami, M., Furukawa, Y., Karasawa, Y., Ren, L.M., Chiba, S. Japanese heart journal. (1990) [Pubmed]
  6. Influence of extracellular H+ and Ca2+ on Ro 22-9194-induced block of sodium current in cardiac myocytes. Hisatome, I., Tanaka, Y., Sasaki, N., Hiroe, K., Ahmmed, G.U., Tsuboi, M., Manabe, I., Suga, T., Yamamoto, Y., Ohtahara, A., Kinugawa, T., Ogino, K., Igawa, O., Yoshida, A., Saito, M., Sato, R., Shigemasa, C. Gen. Pharmacol. (1997) [Pubmed]
 
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