Article date: August 1980
By: A.S. TADEPALLI, in Volume 69, Issue 4, pages 647-650
Vagally mediated reflex bradycardia was elicited in spinal cats with intravenous pressor doses of noradrenaline. Administration of 5‐hydroxytryptophan (1.5 and 3 mg total dose) into the fourth cerebral ventricle reduced the reflex bracycardia.
Inhibition of central amino acid decarboxylase with R044602 prevented the effects of 5‐hydroxytryptophan. After intravenous administration of 5‐hydroxytryptophan, vagal reflex bradycardia was not affected.
Results suggest that 5‐hydroxytryptophan acts in the CNS to inhibit baroreceptor‐mediated vagal reflex bradycardia and that action is mediated via conversion to 5‐hydroxytryptamine.
Vagally mediated reflex bradycardia was elicited in spinal cats with intravenous pressor doses of noradrenaline. Administration of 5‐hydroxytryptophan (1.5 and 3 mg total dose) into the fourth cerebral ventricle reduced the reflex bracycardia.
Inhibition of central amino acid decarboxylase with R044602 prevented the effects of 5‐hydroxytryptophan. After intravenous administration of 5‐hydroxytryptophan, vagal reflex bradycardia was not affected.
Results suggest that 5‐hydroxytryptophan acts in the CNS to inhibit baroreceptor‐mediated vagal reflex bradycardia and that action is mediated via conversion to 5‐hydroxytryptamine.
DOI: 10.1111/j.1476-5381.1980.tb07916.x
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