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Krstić MK, Djurković D. Analysis of the cardiovascular responses to central injection of tryptamine in rats. Neuropharmacology. 1985;24(6):517-25doi: 10.1016/0028-3908(85)90057-7.
Krstić, M. K., & Djurković, D. (1985). Analysis of the cardiovascular responses to central injection of tryptamine in rats. Neuropharmacology, 24(6), 517-25. https://doi.org/10.1016/0028-3908(85)90057-7
Krstić, M K, and Djurković, D. "Analysis of the cardiovascular responses to central injection of tryptamine in rats." Neuropharmacology vol. 24,6 (1985): 517-25. doi: https://doi.org/10.1016/0028-3908(85)90057-7
Krstić MK, Djurković D. Analysis of the cardiovascular responses to central injection of tryptamine in rats. Neuropharmacology. 1985 Jun;24(6):517-25. doi: 10.1016/0028-3908(85)90057-7. PMID: 3160964.
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Neuropharmacology. 1985 Jun;24(6):517-25. doi: 10.1016/0028-3908(85)90057-7.

Analysis of the cardiovascular responses to central injection of tryptamine in rats.

Neuropharmacology

M K Krstić, D Djurković

PMID: 3160964 DOI: 10.1016/0028-3908(85)90057-7

Abstract

Tryptamine (2-20 micrograms), administered into the lateral cerebral ventricle of the rat, evoked a pressor response which was sometimes followed by a prolonged depressor response. The intracisternal administration of tryptamine (7-20 micrograms) caused a slow progressive and long-lasting depressor effect without or with an initial pressor effect. The pressor response was accompanied by variable changes in heart rate, whilst the pure depressor response was accompanied by a decrease in heart rate. After transection of the spinal cord between C1 and C2 the pressor response was substantially reduced or abolished. Methysergide, injected centrally, antagonized in a dose-dependent manner the pressor effect, whilst p-chlorophenylalanine, atropine and hexamethonium, administered by the same route, did not diminish this effect. It is concluded that tryptamine, injected centrally, causes both increases and decreases in arterial blood pressure and heart rate. The pressor response to tryptamine results from the activation of central noncholinergic, methysergide-sensitive, receptor sites and the depressor response to tryptamine may be due to a centrally-induced reduction in sympathetic nervous activity. It is tentatively suggested that tryptamine, like 5-hydroxytryptamine, participates in the physiological regulation of the cardiovascular system of the rat, as both a central excitatory and inhibitory regulator.

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