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Prostacyclin biosynthesis and platelet function in autonomic dysfunction.

M R Goldberg, D Robertson, G A FitzGerald

    Neurology
    |January 1, 1985
    PubMed
    Summary
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    Patients with autonomic dysfunction, including Shy-Drager syndrome and idiopathic orthostatic hypotension, showed normal prostacyclin metabolite levels. Indomethacin treatment did not increase prostacyclin production in these patients.

    Area of Science:

    • Cardiovascular Physiology
    • Endocrinology
    • Autonomic Nervous System Disorders

    Background:

    • Prostacyclin is a vasodilator prostanoid involved in blood pressure regulation.
    • Autonomic dysfunction, seen in Shy-Drager syndrome and idiopathic orthostatic hypotension, can lead to orthostatic hypotension.
    • The role of prostacyclin in the pathophysiology of these conditions is not fully understood.

    Purpose of the Study:

    • To investigate urinary prostacyclin metabolite (PGI-M) excretion in patients with Shy-Drager syndrome and idiopathic orthostatic hypotension.
    • To determine the effect of indomethacin, a prostaglandin synthesis inhibitor, on blood pressure and PGI-M excretion in these patients.

    Main Methods:

    • Urinary PGI-M levels were measured in patients before and after indomethacin administration.

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  • Blood pressure response to indomethacin was monitored.
  • Platelet aggregation was assessed in some subjects.

    • Main Results:

    • Urinary PGI-M excretion was within the normal range in patients with autonomic dysfunction.
    • Indomethacin administration caused a significant rise in blood pressure.
    • Urinary PGI-M excretion decreased by 57% after indomethacin treatment, indicating suppressed prostaglandin synthesis.
    • No circulating inhibitors of platelet aggregation were found during induced hypotension.

    Conclusions:

    • Patients with Shy-Drager syndrome and idiopathic orthostatic hypotension do not exhibit increased prostacyclin production.
    • Indomethacin's efficacy in raising blood pressure in these patients is not mediated by enhanced prostacyclin production.
    • The findings suggest that prostacyclin may not play a significant role in the compensatory mechanisms for hypotension in these autonomic disorders.