[A MODULATORY INFLUENCE OF THE iNOS ON THE FUNCTIONAL ACTIVITY OF THE KATP-CHANNELS IN CORONARY VESSELS OF RATS ADAPTED TO THE STRESS]

Ross Fiziol Zh Im I M Sechenova. 2016 Jul;102(7):864-75.
[Article in Russian]

Abstract

In the experiments carried out on the isolated by Langendorff's method hearts which were perfused at the constant coronary flow it was studied influence of iNOS-derived NO on the functional activity of the KATP-channels in the coronary vascular smooth muscle cells following formation of the adaptation to the stress. As an adaptation to the short stress as a 6-hours immobilization stress result in increase of NO production and rise of expression of gene iNOS; however, adaptation in contrast to the stress leads to moderate accumulation of iNOS against the background unchanged systemic activity of еNOS and in the absence of systemic low-grade inflammation. After an adaptation to the short stress or after 6 hours of immobilization the functional glybenclamid-inhibiting activity of the KATP-channels was suppressed. Nevertheless, after prolonged immobilization suppressed activity of the channels was abolished after blockage of iNOS, whereas iNOS blockage in adapted animals leads not only to the recovery but even to the hyperactivation of the KATP-channels. Hence, increase in NO production which is typical for the adaptation, limits activation of the KATP-channels thus creating a strong link between these channels activity and NO produced by iNOS.

MeSH terms

  • Adaptation, Physiological
  • Animals
  • Animals, Outbred Strains
  • Coronary Vessels / drug effects
  • Coronary Vessels / enzymology*
  • Endothelium, Vascular / drug effects
  • Endothelium, Vascular / enzymology*
  • Enzyme Inhibitors / pharmacology
  • Female
  • Gene Expression Regulation
  • Glyburide / pharmacology
  • Heart / drug effects
  • Heart / physiopathology
  • Immobilization / methods
  • Isothiuronium / analogs & derivatives
  • Isothiuronium / pharmacology
  • KATP Channels / antagonists & inhibitors
  • KATP Channels / genetics
  • KATP Channels / metabolism*
  • Myocytes, Smooth Muscle / drug effects
  • Myocytes, Smooth Muscle / metabolism
  • Nitric Oxide / antagonists & inhibitors
  • Nitric Oxide / metabolism*
  • Nitric Oxide Synthase Type II / antagonists & inhibitors
  • Nitric Oxide Synthase Type II / genetics
  • Nitric Oxide Synthase Type II / metabolism*
  • Nitric Oxide Synthase Type III / genetics
  • Nitric Oxide Synthase Type III / metabolism
  • Organ Culture Techniques
  • Perfusion
  • Potassium Channel Blockers / pharmacology
  • Rats
  • Stress, Psychological / enzymology*
  • Stress, Psychological / genetics
  • Stress, Psychological / physiopathology

Substances

  • Enzyme Inhibitors
  • KATP Channels
  • Potassium Channel Blockers
  • Isothiuronium
  • Nitric Oxide
  • Nitric Oxide Synthase Type II
  • Nitric Oxide Synthase Type III
  • Nos2 protein, rat
  • Nos3 protein, rat
  • S-methylisothiopseudouronium
  • Glyburide