Inhibition of platelet aggregation and the stimulation of prostacyclin synthesis by insulin in humans

N. N. Kahn, W. A. Bauman, V. B. Hatcher, A. K. Sinha

Research output: Contribution to journalArticlepeer-review

34 Scopus citations


An intravenous bolus injection of insulin (35.5 μM) followed by an infusion of insulin (0.53 μM · kg-1 · h-1) for 2.5 h (which maintained plasma levels between 0.71 nM to 1.4 nM) in normal fasting volunteers (n = 16), increased [3H]-prostaglandin E1 (a probe for prostacyclin) binding to platelets by two- to threefold over the control. Scatchard analyses showed that the increased binding was due to the increase of both high and low affinity receptor numbers with little change in the receptor affinities. Similar results were obtained by using [3H]prostacyclin as the radioligand. The increased binding was associated with more than a twofold decrease of the minimum concentration of prostanoid needed to inhibit aggregation of platelets through the increased formation of adenosine 3',5'-cyclic monophosphate. Furthermore, the infusion increased the mean plasma prostacyclin level from 12.10 ± 4.5 pM to 23.9 ± 6.7 pM (n = 16; P < 0.001). These effects of insulin were at least partially direct, since the treatment of endothelial cells with insulin in tissue culture stimulated the production of the autacoid. Bolus injection of insulin (0.71 μM/kg) showed that the above effects of insulin could be demonstrated within 20 min after the injection, attained maximal ranges in ~60 min, and disappeared by 2-4 h.

Original languageEnglish (US)
Pages (from-to)H2160-H2167
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Issue number6 34-6
StatePublished - 1993
Externally publishedYes


  • adenosine 3',5'-cyclic monophosphate
  • endothelial cells
  • prostaglandin receptors
  • serotonin release

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)


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