The influence of serotonin on intravascular volume in the total capacitance circulation has not previously been examined. Thus blood was drained from the venae cavae to an extracorporeal reservoir and returned to the right atrium at a constant rate so that total intravascular volume changes could be recorded as the inverse of changes in reservoir volume in 31 anaesthetized dogs. Serotonin (588 ± 47 μg) in the left atrium was associated with an initial decrease in intravascular volume of 39 ± 12 ml (P < 0.01) followed by an increase of 129 ± 31 ml (P < 0.01) above control at 20 min. Mean arterial pressure increased from a control of 74 ± 4 mmHg to 99 ± 7 mmHg (P < 0.01) initially and then decreased to 64 ± 5 mmHg (P < 0.05) at 20 min. Following ganglionic blockade with mecamylamine, serotonin caused only a decrease in intravascular volume, which was 73 ± 12 ml (P < 0.01) at 20 min. 5-HT2 and α-adrenergic blockade with ketanserin did not attenuate the early decrease in intravascular volume. 5-Carboxamidotryptamine (82 ± 39 μg), a 5-HT1 agonist, was associated with only an increase in intravascular volume, which was 82 ± 13 ml (P < 0.01) at 20 min and which was abolished after ganglionic blockade. Thus, serotonin causes a biphasic change in total intravascular volume. The initial decrease in intravascular volume is not mediated by a reflex or by 5-HT1, 5-HT2, or α-adrenergic receptor stimulation. The late intravascular volume increment appears to be mediated, at least in part, by preganglionic or ganglionic stimulation, which may well be at a 5-HT1 receptor. In an animal with an intact circulation, the biphasic volume change might be expected to act via the Starling mechanism to first increase and then decrease cardiac output and thereby enhance the effect of the biphasic total peripheral resistance change on arterial pressure.
|Original language||English (US)|
|Number of pages||8|
|Journal||Acta Physiologica Scandinavica|
|State||Published - 1990|
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