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Hypotensive and bradycardic effects of dl-tetrahydropalmatine mediated by decrease in hypothalamic serotonin release

F Y Chueh¹, M T Hsieh, C F Chen

¹Institute of Chinese Pharmaceutical Sciences, China Medical College, Taichung, Taiwan.

Japanese Journal of Pharmacology

|October 1, 1995

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dl-tetrahydropalmatine (dl-THP) reduces blood pressure and heart rate by decreasing hypothalamic serotonin release. This effect was reversed by stimulating serotonin receptors, indicating a key role for serotonin in dl-THP

Area of Science:

Neuropharmacology
Cardiovascular Physiology

Background:

Serotonin (5-HT) plays a complex role in regulating cardiovascular function.
Hypothalamic serotonin pathways are implicated in blood pressure and heart rate control.

Purpose of the Study:

To investigate the effects of dl-tetrahydropalmatine (dl-THP) on cardiovascular parameters.
To elucidate the role of hypothalamic serotonin in dl-THP-induced cardiovascular changes.

Main Methods:

Intravenous administration of dl-THP in anesthetized rats.
Measurement of hypothalamic serotonin release using carbon-fiber electrodes and voltammetry.
Pharmacological manipulation of serotonin 5-HT2 receptors using cyproheptadine, ketanserin, and DOI.

Main Results:

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dl-THP administration caused dose-dependent hypotension, bradycardia, and decreased hypothalamic serotonin release.
Blockade of 5-HT2 receptors mimicked dl-THP effects, while stimulation with DOI produced hypertension and tachycardia.
DOI treatment reversed dl-THP-induced hypotension and bradycardia.

Conclusions:

dl-tetrahydropalmatine decreases arterial pressure and heart rate.
These cardiovascular effects are mediated by a reduction in hypothalamic serotonin release.
Serotonergic pathways in the hypothalamus are critical for dl-THP's cardiovascular actions.