Abstract
In the Gulf toadfish (
Opsanus beta
), the serotonin (5-HT) transporter (SERT) is highly expressed in the heart, and the heart and gill both demonstrate the capacity for SERT-mediated uptake of 5-HT from the circulation. Because 5-HT is a potent vasoconstrictor in fish, we hypothesized that hypoxia exposure may increase 5-HT uptake by these tissues—and increase excretion of 5-HT—to prevent branchial vasoconstriction that would hamper gas exchange. Spot sampling of blood, bile, and urine revealed that fish exposed to chronic hypoxia (1.83 ± 0.12 mg·L
−1
O
2
for 24–26 h) had 41% lower plasma 5-HT in the ventral aorta (immediately following the heart) than in the hepatic vein (immediately before the heart), suggesting enhanced cardiac 5-HT uptake during hypoxia. 5-HT concentrations in the bile were greater than those in the urine, but there were no effects of acute (1.31 ± 0.06 mg·L
−1
O
2
for 25 min) or chronic hypoxia on 5-HT levels in these fluids. In 5-HT radiotracer experiments, the presence of tracer in the bile decreased upon hypoxia exposure, but, surprisingly, neither acute nor chronic hypoxia-induced changes in [
3
H]5-HT uptake in the heart, gill, or other tissues. Given the likely impact of the hypoxia exposure on metabolic rate, future studies should examine the effects of a milder hypoxia exposure on 5-HT uptake into these tissues and the role of 5-HT degradation.
