Inhibition of crossbridge function in the normal human heart by hypoxic endothelial superfusate

Biochem Biophys Res Commun. 1999 Aug 19;262(1):64-7. doi: 10.1006/bbrc.1999.1058.

Abstract

Endothelial cells release diffusible substances which modulate myocardial function. Oxygen pressure is one important factor for stimulation and modulation of endothelial function. Here we investigated the effects of a superfusate obtained from hypoxic (pO(2) 40-50 mmHg) porcine endothelial cell culture on human myocardial crossbridge cycling rate. Isometric force development and the rate constant for tension development of demembranated multicellular fibers from the left myocardium of a normal human heart were determined from the low-tension rigor by photolytic release of ATP from caged-ATP. Incubation with hypoxic or normoxic superfusates did not change maximal isometric force development. However, rate constant of tension development of the normal human heart fibers significantly decreased to 43.3% upon incubation with the hypoxic but not normoxic endothelial cell superfusate.

MeSH terms

  • Adenosine Triphosphate / analogs & derivatives
  • Adenosine Triphosphate / metabolism
  • Animals
  • Calcium / metabolism
  • Cell Hypoxia / physiology*
  • Cells, Cultured
  • Culture Media, Conditioned / pharmacology
  • Endothelium, Vascular / cytology
  • Endothelium, Vascular / metabolism*
  • Heart / physiology*
  • Humans
  • Kinetics
  • Muscle Fibers, Skeletal / cytology
  • Muscle Fibers, Skeletal / metabolism
  • Myocardial Contraction*
  • Myocardium / cytology
  • Myocardium / metabolism
  • Myosins / metabolism*
  • Photolysis
  • Swine

Substances

  • Culture Media, Conditioned
  • P(3)-1-(2-nitro)phenylethyladenosine 5'-triphosphate
  • Adenosine Triphosphate
  • Myosins
  • Calcium