Prostacyclin and thromboxane A2 formation in response to adrenergic stimulation in humans: a mechanism for local control of vascular response to sympathetic activation?

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Abstract
Prostacyclin (PGI2) and thromboxane A2 (TxA2), antiaggregating and aggregating agents, may be involved in the control of local vasomotor tone owing to their vasoactive properties. In 15 healthy young volunteers, circulating PGI2 (biological assay using superfusion technique) and plasma TxA2 levels (measured by radioimmunoassay as its stable derivative TxB2) have been investigated. Adrenergic stimulation was induced by a 2 min cold application and its effectiveness was checked in all subjects by the changes in forearm calculated vascular resistance (blood flow was measured by strain gauge plethysmography), and in six subjects by changes in catecholamine plasma levels (radioenzymatic assay). Cold application induced a sharp increase in calculated vascular resistance and plasma noradrenaline concentration in all subjects. Adrenergic stimulation was associated with a prompt elevation of circulating PGI2 (from 6.67 ± 2.38 to 12.18 ± 2.95 ng·cm−3, P < 0.001) and TxB2 levels (from 0.49 ± 0.18 to 1.10 ± 0.61 pmol·cm−3, P < 0.001). PGI2 and TxB2 increases disappeared within 10 min. In subjects treated with 5 mg·kg−1 ASA, both TxB2 resting levels and their increase after adrenergic stimulation were not significantly different from values before ASA although platelets were unable to produce TxB2. Therefore, platelets were not the source of TxB2 in plasma. After 10 mg·kg−1 ASA, TxB2 increase following adrenergic stimulation was unaffected whereas PGI2 elevation was completely blocked and the increase in calculated vascular resistance was significantly higher than in subjects pretreated with saline. These findings indicate that TxB2 and PGI2 formation may represent a modulating mechanism of vascular response to adrenergic stimulation.

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