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Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation.
J Pharmacol Exp Ther. 1984 Jun; 229(3):816-22.JP

Abstract

The vasoconstrictor response to 5-hydroxytryptamine (5-HT) released from vascular adrenergic nerves by periarterial nerve stimulation (PNS) was studied in the perfused mesenteric vascular bed isolated from the rat. PNS was delivered at 4 to 16 Hz, 2 msec in pulse duration for 30 sec. After treatment with 5-HT (1 and 10 microM) for 20 min, the pressor response to PNS, previously decreased by 80 to 90% with phentolamine (0.1 microM), was greatly potentiated and a frequency-dependent pressor response to PNS reappeared. However, the 5-HT treatment did not alter the pressor response to infusion of exogenous norepinephrine (0.5 and 1 nmol) previously decreased by phentolamine. This potentiation did not occur in the presence of methysergide (0.1 microM), ketanserin (0.1 microM), tetrodotoxin (0.1 microM), guanethidine (5 microM) or in Ca++-free Krebs' solution. Also, in the preparation treated with 6-hydroxydopamine, 5-HT treatment had no effect on the abolished PNS response. Either cocaine (10 microM) or fluoxetine (10 microM) but not corticosterone (10 microM) prevented the potentiation when perfused together with 5-HT. In the mesenteric vascular bed prelabeled with [3H]-5-HT, PNS evoked a frequency-dependent increase of tritium efflux, which was abolished by treatment with tetrodotoxin guanethidine or 6-hydroxydopamine and in Ca++-free Krebs' solution. These results suggest that 5-HT is taken up by vascular adrenergic nerve endings in vitro and it is released by nerve stimulation, resulting in vasoconstriction. It is also suggested that 5-HT may contribute to the maintenance of local vascular tone through this mechanism in vivo.

Authors

No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

6427449

Citation

Kawasaki, H, and K Takasaki. "Vasoconstrictor Response Induced By 5-hydroxytryptamine Released From Vascular Adrenergic Nerves By Periarterial Nerve Stimulation." The Journal of Pharmacology and Experimental Therapeutics, vol. 229, no. 3, 1984, pp. 816-22.
Kawasaki H, Takasaki K. Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation. J Pharmacol Exp Ther. 1984;229(3):816-22.
Kawasaki, H., & Takasaki, K. (1984). Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation. The Journal of Pharmacology and Experimental Therapeutics, 229(3), 816-22.
Kawasaki H, Takasaki K. Vasoconstrictor Response Induced By 5-hydroxytryptamine Released From Vascular Adrenergic Nerves By Periarterial Nerve Stimulation. J Pharmacol Exp Ther. 1984;229(3):816-22. PubMed PMID: 6427449.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Vasoconstrictor response induced by 5-hydroxytryptamine released from vascular adrenergic nerves by periarterial nerve stimulation. AU - Kawasaki,H, AU - Takasaki,K, PY - 1984/6/1/pubmed PY - 1984/6/1/medline PY - 1984/6/1/entrez SP - 816 EP - 22 JF - The Journal of pharmacology and experimental therapeutics JO - J Pharmacol Exp Ther VL - 229 IS - 3 N2 - The vasoconstrictor response to 5-hydroxytryptamine (5-HT) released from vascular adrenergic nerves by periarterial nerve stimulation (PNS) was studied in the perfused mesenteric vascular bed isolated from the rat. PNS was delivered at 4 to 16 Hz, 2 msec in pulse duration for 30 sec. After treatment with 5-HT (1 and 10 microM) for 20 min, the pressor response to PNS, previously decreased by 80 to 90% with phentolamine (0.1 microM), was greatly potentiated and a frequency-dependent pressor response to PNS reappeared. However, the 5-HT treatment did not alter the pressor response to infusion of exogenous norepinephrine (0.5 and 1 nmol) previously decreased by phentolamine. This potentiation did not occur in the presence of methysergide (0.1 microM), ketanserin (0.1 microM), tetrodotoxin (0.1 microM), guanethidine (5 microM) or in Ca++-free Krebs' solution. Also, in the preparation treated with 6-hydroxydopamine, 5-HT treatment had no effect on the abolished PNS response. Either cocaine (10 microM) or fluoxetine (10 microM) but not corticosterone (10 microM) prevented the potentiation when perfused together with 5-HT. In the mesenteric vascular bed prelabeled with [3H]-5-HT, PNS evoked a frequency-dependent increase of tritium efflux, which was abolished by treatment with tetrodotoxin guanethidine or 6-hydroxydopamine and in Ca++-free Krebs' solution. These results suggest that 5-HT is taken up by vascular adrenergic nerve endings in vitro and it is released by nerve stimulation, resulting in vasoconstriction. It is also suggested that 5-HT may contribute to the maintenance of local vascular tone through this mechanism in vivo. SN - 0022-3565 UR - https://www.unboundmedicine.com/medline/citation/6427449/Vasoconstrictor_response_induced_by_5_hydroxytryptamine_released_from_vascular_adrenergic_nerves_by_periarterial_nerve_stimulation_ L2 - https://jpet.aspetjournals.org/cgi/pmidlookup?view=long&pmid=6427449 DB - PRIME DP - Unbound Medicine ER -