A further study of the vasodilator and negative inotropic mechanisms of action of nicorandil and its congeners in the canine heart

@article{Satoh2004AFS,
  title={A further study of the vasodilator and negative inotropic mechanisms of action of nicorandil and its congeners in the canine heart},
  author={Keisuke Satoh and Kensuke Orito and Fumiya Yoneyama and Norio Taira},
  journal={Cardiovascular Drugs and Therapy},
  year={2004},
  volume={8},
  pages={227-234}
}
  • K. Satoh, K. Orito, N. Taira
  • Published 1 April 1994
  • Medicine, Chemistry, Biology
  • Cardiovascular Drugs and Therapy
SummaryThe vasodilator and negative inotropic mechanisms of action of nicorandil and its congeners (SG-209, SG-103, and SG-86) were investigated in isolated canine papillary muscle preparations cross-circulated through the anterior septal artery with support dogs. SG-209, SG-103, and SG-86 were obtained by replacement of the nitroxyl group of nicorandil by acetoxyl, nicotinoyloxyl, and hydroxyl groups, respectively. Nicorandil (0.03–10 µmol), SG-209 (0.1–10 µmol), SG-103 (1–30 µmol), and SG-86… 
Pharmacokinetics of nicorandil in dogs with mild mitral regurgitation.

References

SHOWING 1-10 OF 21 REFERENCES
The group at C2 of N-ethylnicotinamide determines the vasodilator potencies and mechanisms of action of nicorandil and its congeners in canine coronary arteries
TLDR
The results indicate that the group at C2 of the parent structure of nicorandil and its congeners, i.e., N-ethylnicotinamide determines not only the vasodilator potency but the vasODilator mechanism of action of the compound.
Effect of 2-nicotinamidethyl nitrate (SG 75) on coronary circulation.
TLDR
The results indicate that SG 75 is a potent and long-acting coronary vasodilating agent and it causes an increase in blood flow of constricted as well as non-constricted coronary artery.
Cyclic GMP as Possible Mediator of Coronary Arterial Relaxation by Nicorandil (SG‐75)
  • S. Holzmann
  • Biology
    Journal of cardiovascular pharmacology
  • 1983
TLDR
Results indicate that nicorandil relaxes vascular smooth muscle, at least in part, through cGMP, which is likely to be mediated by cyclic GMP.
Spasmolytic Action of Nicorandil in Canine Conductive Coronary Arteries In Vivo Is Not Modified by Glibenclamide
TLDR
The results suggest that the spasmolytic effect of nicorandil on canine conductive coronary vessels is not mediated by K-channel opening but by a nitroglycerin-like action and that the dilatation of resistive coronary arteries induced by nicor andil may be largely due to its action as a K- channel opener.
Nicorandil increases coronary blood flow predominantly by K-channel opening mechanism
TLDR
The results indicate that the effect of nicorandil in increasing coronary blood flow, like that of cromakalim, is predominantly due to its mechanism of action as a K-channel opener.
The negative inotropic effect of nicorandil is independent of cyclic GMP changes: a comparison with pinacidil and cromakalim in canine atrial muscle
TLDR
It is concluded that the negative inotropic effects of nicorandil like those of cromakalim and pinacidil do not result from an increase in cyclic GMP concentrations, and instead these effects may be due to their action as K‐channel openers.
Differential antagonism by glibenclamide of the relaxant effects of cromakalim, pinacidil and nicorandil on canine large coronary arteries
TLDR
In canine large epicardial coronary arteries cromakalim produced relaxation by the mechanism antagonized by glibenclamide, probably opening ATP-sensitive potassium channels, pinacidil and nicorandil did so by the mechanisms shared with cromkalim and by one not antagonizedby glibanclamide as well, and Nicorandils did so exclusively by the mode of action as a nitrate.
Specific but differential antagonism by glibenclamide of the vasodepressor effects of cromakalim and nicorandil in spinally‐anaesthetized dogs
TLDR
The results suggest that the vasodepressor action of cromakalim is due predominantly to potassium channelOpening, but that of nicorandil involves not only potassium channel opening but its action as a nitrate.
Is the Cardiovascular Profile of BRL 34915 Characteristic of Potassium Channel Activators?
TLDR
The cardiac effects of BRL 34915 are very similar to those of nicorandil and pinacidil, whose cardiac effects result exclusively from an increase in membrane K conductance in cardiac muscle cells, and were highly vasoselective.
Interaction of potassium channel openers and blockers in canine atrial muscle
TLDR
Quaternary ammonium compounds like TEA and TBA antagonize the negative inotropic effect of cromakalim, pinacidil and nicorandil by binding to potassium channels, thus preventing binding of the channel openers to the same sites or closely related sites in canine right atrial muscles.
...
...