Insulin, cortisol and catecholamines do not regulate circadian variations in fibrinolytic activity

Wayne L. Chandler, Dan Mornin, Richard O. Whitten, Peter Angleton, Federico M. Farin, Thomas R. Fritsche, Richard C. Veith, John R. Stratton

Research output: Contribution to journalArticlepeer-review

32 Scopus citations


To evaluate possible hormonal regulators of the diurnal rhythm in fibrinolytic activity, we measured tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor activity (PAI-1), t-PA antigen, insulin, cortisol, and catecholamines in 6 healthy males (age 34±5) every 2 hours for 24 hours. Fibrinolysis was characterized by a peak in PAI-1 activity and a trough in t-PA activity at 0600 h. PAI-1 activity increased 92% and t-PA activity decreased 56% between 2400 h and 0600 h. t-PA antigen (principally a measure of t-PA/PAI-1 complex), peaked at 0800 h. In comparison, insulin levels were lowest at night when PAI-1 activity was rising. The weak inverse correlation between insulin and PAI-1 activity (r = -0.28, p < 0.02), was not sufficient to explain the diurnal change in fibrinolysis. While cortisol demonstrated the expected circadian change, the increase in cortisol did not occur until 0400 h, 4-6 hours after the rise in PAI-1 and decrease in t-PA activity started. Supine resting plasma epinephrine and norepinephrine showed no circadian rhythm. From this data, we hypothesize that the increased level of PAI-1 in the morning consumes t-PA, leading to decreased t-PA activity and increased t-PA/PAI-1 complex. Further, we conclude that insulin, cortisol, and catecholamines are not responsible for the circadian rhythm of fibrinolysis.

Original languageEnglish (US)
Pages (from-to)1-12
Number of pages12
JournalThrombosis Research
Issue number1
StatePublished - Apr 1 1990


  • catecholamine
  • circadian rhythm
  • cortisol
  • fibrinolysis
  • insulin

ASJC Scopus subject areas

  • Hematology
  • Cardiology and Cardiovascular Medicine


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