Induction of resistance to endothelin-1's biochemical actions by elevated glucose levels in retinal pericytes

Diabetes. 1992 Dec;41(12):1533-9. doi: 10.2337/diabetes.41.12.1533.

Abstract

Because retinal pericytes have contractile properties and are affected by diabetes, we have studied the responsiveness of pericytes to ET-1, a potent vasoconstrictor, in the presence of various concentrations of glucose. Cultured calf retinal pericytes were exposed to glucose levels of 5.5 or 25 mM for up to 8 days. Radioreceptor studies that used [125I]ET-1 showed that pericytes contained high-affinity binding sites with Kd of 3 x 10(-10) M, and these binding affinities were unaffected by glucose concentration. Receptor number appears to be elevated, but this increase was NS. Responsiveness of pericytes to ET-1 was studied with respect to stimulation of DAG and IP3 levels and PKC activities. In contrast to receptor binding, exposure to 25 mM glucose for > 6 days blunted pericyte responsiveness to ET-1. The time course of ET-1 stimulation as measured by [3H]glycerol labeling, and IP3 level showed a 98% increase in [3H]DAG at 10 min and a fourfold increase for IP3, respectively. Cells exposed to 25 mM glucose only had a 32% increase for DAG, and no increase for IP3 was observed. Dose-response studies on the stimulation of [3H]DAG increase showed the range of ET-1's effect to be between 10(-9) and 10(-7) M. At maximum, cells exposed to 5.5 mM glucose had a 70% increase versus only a 30% increase in those exposed to 25 mM glucose. Similarly, ET-1 only increased the total DAG levels in pericytes exposed to 5.5 mM glucose by 41%. PKC activity also was measured because DAG is one of its cellular activators.(ABSTRACT TRUNCATED AT 250 WORDS)

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Arterioles / cytology
  • Arterioles / drug effects
  • Arterioles / metabolism*
  • Cattle
  • Cells, Cultured
  • Diglycerides / metabolism*
  • Drug Resistance
  • Endothelins / metabolism
  • Endothelins / pharmacology*
  • Glucose / pharmacology*
  • Inositol 1,4,5-Trisphosphate / metabolism*
  • Muscle, Smooth, Vascular / cytology
  • Muscle, Smooth, Vascular / drug effects
  • Muscle, Smooth, Vascular / metabolism*
  • Protein Kinase C / isolation & purification
  • Protein Kinase C / metabolism*
  • Receptors, Endothelin / metabolism*
  • Retina / physiology*

Substances

  • Diglycerides
  • Endothelins
  • Receptors, Endothelin
  • Inositol 1,4,5-Trisphosphate
  • Protein Kinase C
  • Glucose