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Reciprocal potentiation of a vasoconstrictor response between 5-hydroxytryptamine and clonidine in the perfused mesenteric vascular bed of the rat.
Arch Int Pharmacodyn Ther. 1987 May; 287(1):16-30.AI

Abstract

The interaction between 5-hydroxytryptamine (5-HT) and clonidine, an alpha 2-adrenoceptor agonist, was investigated in the isolated perfused mesenteric vascular bed of the rat. Clonidine itself did not cause vasoconstriction even at 300 micrograms. However, clonidine in the presence of 5-HT (10 and 100 nM) caused a marked vasoconstriction in a dose range of 0.1 micrograms to 300 micrograms. Prazosin inhibited the clonidine response, whereas yohimbine did not. The potency of prazosin against clonidine was less than that against an alpha 1-adrenoceptor agonist phenylephrine. Therefore, it is suggested that clonidine activated alpha 1-like adrenoceptors. 5-HT also potentiated the vasoconstrictor response to perivascular nerve stimulation, exogenous norepinephrine (NE) and phenylephrine. Calcium entry blockade by nicardipine (0.1 microM) reduced the response to clonidine in the presence of 5-HT, whereas that to phenylephrine in the presence or absence of 5-HT was not reduced. On the other hand, clonidine (0.01-1 microM) potentiated the vasoconstrictor effect of 5-HT more than NE did. Ouabain (1 microgram/ml) enabled clonidine to exhibit an agonistic action, and also enhanced the contractile response to 5-HT. In conclusion, 5-HT modulated the vasoconstrictor effect of clonidine, and the vasoconstriction with 5-HT was also facilitated by clonidine reciprocally. It is possible that a partial depolarization of the cell membrane is the common mechanism for their reciprocal potentiation.

Authors

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Pub Type(s)

Journal Article

Language

eng

PubMed ID

3477130

Citation

Takiguchi, Y, et al. "Reciprocal Potentiation of a Vasoconstrictor Response Between 5-hydroxytryptamine and Clonidine in the Perfused Mesenteric Vascular Bed of the Rat." Archives Internationales De Pharmacodynamie Et De Therapie, vol. 287, no. 1, 1987, pp. 16-30.
Takiguchi Y, Hashimoto H, Nakashima M. Reciprocal potentiation of a vasoconstrictor response between 5-hydroxytryptamine and clonidine in the perfused mesenteric vascular bed of the rat. Arch Int Pharmacodyn Ther. 1987;287(1):16-30.
Takiguchi, Y., Hashimoto, H., & Nakashima, M. (1987). Reciprocal potentiation of a vasoconstrictor response between 5-hydroxytryptamine and clonidine in the perfused mesenteric vascular bed of the rat. Archives Internationales De Pharmacodynamie Et De Therapie, 287(1), 16-30.
Takiguchi Y, Hashimoto H, Nakashima M. Reciprocal Potentiation of a Vasoconstrictor Response Between 5-hydroxytryptamine and Clonidine in the Perfused Mesenteric Vascular Bed of the Rat. Arch Int Pharmacodyn Ther. 1987;287(1):16-30. PubMed PMID: 3477130.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Reciprocal potentiation of a vasoconstrictor response between 5-hydroxytryptamine and clonidine in the perfused mesenteric vascular bed of the rat. AU - Takiguchi,Y, AU - Hashimoto,H, AU - Nakashima,M, PY - 1987/5/1/pubmed PY - 1987/5/1/medline PY - 1987/5/1/entrez SP - 16 EP - 30 JF - Archives internationales de pharmacodynamie et de therapie JO - Arch Int Pharmacodyn Ther VL - 287 IS - 1 N2 - The interaction between 5-hydroxytryptamine (5-HT) and clonidine, an alpha 2-adrenoceptor agonist, was investigated in the isolated perfused mesenteric vascular bed of the rat. Clonidine itself did not cause vasoconstriction even at 300 micrograms. However, clonidine in the presence of 5-HT (10 and 100 nM) caused a marked vasoconstriction in a dose range of 0.1 micrograms to 300 micrograms. Prazosin inhibited the clonidine response, whereas yohimbine did not. The potency of prazosin against clonidine was less than that against an alpha 1-adrenoceptor agonist phenylephrine. Therefore, it is suggested that clonidine activated alpha 1-like adrenoceptors. 5-HT also potentiated the vasoconstrictor response to perivascular nerve stimulation, exogenous norepinephrine (NE) and phenylephrine. Calcium entry blockade by nicardipine (0.1 microM) reduced the response to clonidine in the presence of 5-HT, whereas that to phenylephrine in the presence or absence of 5-HT was not reduced. On the other hand, clonidine (0.01-1 microM) potentiated the vasoconstrictor effect of 5-HT more than NE did. Ouabain (1 microgram/ml) enabled clonidine to exhibit an agonistic action, and also enhanced the contractile response to 5-HT. In conclusion, 5-HT modulated the vasoconstrictor effect of clonidine, and the vasoconstriction with 5-HT was also facilitated by clonidine reciprocally. It is possible that a partial depolarization of the cell membrane is the common mechanism for their reciprocal potentiation. SN - 0003-9780 UR - https://www.unboundmedicine.com/medline/citation/3477130/Reciprocal_potentiation_of_a_vasoconstrictor_response_between_5_hydroxytryptamine_and_clonidine_in_the_perfused_mesenteric_vascular_bed_of_the_rat_ DB - PRIME DP - Unbound Medicine ER -