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Yu S. M. – One of the best experts on this subject based on the ideXlab platform.

  • Thaliporphine selectively inhibits expression of the inducible, but not the constitutive, nitric oxide synthase.
    , 1994
    Co-Authors: Yu S. M.

    Abstract:

    Formation of nitrites/nitrates caused by lipopolysaccharide (LPS) in J774.2 macrophages was inhibited by thaliporphine, an Aporphine Derivative isolated from the plant Neolitsea konishii K. This inhibition of nitrite synthesis in LPS-stimulated macrophages by thaliporphine was similar to that by cycloheximide, NG-methyl-L-arginine (MeArg) and dexamethasone. Thaliporphine, but not MeArg, inhibited expression of inducible NO synthase without directly affecting enzyme activity. However, thaliporphine did not inhibit nitrite production by NO synthase that had already been induced by prior exposure to LPS for which any possible further induction was inhibited by cycloheximide. In endothelial cells, nitrite formation induced by bradykinin (in the presence of 0.2 mM Ca2+) was inhibited by MeArg. However, incubation of endothelial cells with dexamethasone, cycloheximide and thaliporphine did not affect this Ca(2+)-dependent nitrite production. Thaliporphine (0.1-100 microM) dose-dependently inhibited nitrite accumulation in macrophages stimulated by interleukin-1 beta (IL-1 beta) whereas nitrite formation induced by tumour necrosis factor alpha was not inhibited. LPS-stimulated IL-1 beta synthesis in macrophages was significantly inhibited by thaliporphine, but thaliporphine had only minimal effect on LPS-stimulated IL-1 beta synthesis in endothelial cells. These results demonstrate that thaliporphine inhibits LPS induction of NO synthase expression, and that the mechanism of action of thaliporphine is via inhibition of LPS-stimulated IL-1 beta synthesis in macrophages. In anaesthetized rats subjected to LPS, pretreatment with thaliporphine partially restored the fall in mean arterial pressure and the vascular hyporeactivity to noradrenaline 3 h after LPS injection. In conclusion, thaliporphine selectively inhibited expression of inducible NO synthase, and may thus hold potential for the treatment of endotoxaemia

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  • Haemodynamic effects of dicentrine, a novel alpha 1-adrenoceptor antagonist: comparison with prazosin in spontaneously hypertensive and normotensive Wistar-Kyoto rats.
    , 1
    Co-Authors: Yu S. M., Hsu S. Y., Ko F. N., Chen C. C., Huang Y. L., Huang T. F., Teng C. M.

    Abstract:

    1. The haemodynamic effects of dicentrine, an Aporphine Derivative isolated from the plant Lindera megaphylla, were investigated and compared with prazosin in rats. 2. In anaesthetized normotensive Wistar-Kyoto (WKY) rats, i.v. administration of dicentrine (0.1, 0.5, 1.0 mg kg-1) and prazosin (0.01, 0.05, 0.1 mg kg-1) induced a dose-related reduction of mean arterial pressure (MAP) which reached a maximal effect 5-10 min after injection and persisted for 2 h. 3. In anaesthetized WKY rats, a higher dose of dicentrine (1.0 mg kg-1, i.v.) did not cause any significant changes in heart rate (HR), cardiac output (CO) and stroke volume (SV) but markedly increased tail blood flow. In contrast, a higher dose of prazosin (0.1 mg kg-1, i.v.) produced a decrease in HR which paralleled the time course of the hypotensive response. 4. The hypotensive activity of dicentrine was completely abolished by alpha-adrenoceptor blockade. Both dicentrine and prazosin significantly attenuated pressor responses to noradrenaline but failed, even at maximal hypotensive doses, to impair the pressor effects of angiotensin II or vasopressin. These observations suggest that dicentrine appears to exert its hypotensive action through alpha 1-adrenoceptor blockade. 5. In conscious normotensive and spontaneously hypertensive (SH) rats, dicentrine (0.5-2.0 mg kg-1, i.v.) and prazosin (0.05-0.2 mg kg-1, i.v.) also evoked dose-related decreases in MAP which were of greater magnitude in SH rats. Oral administration of dicentrine (5 and 8 mg kg-1) to conscious SH rats caused a hypotensive effect which persisted for over 15 h.(ABSTRACT TRUNCATED AT 250 WORDS

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Bruce K. Cassels – One of the best experts on this subject based on the ideXlab platform.

  • Dopaminergic pharmacology and antioxidant properties of pukateine, a natural product lead for the design of agents increasing dopamine neurotransmission
    General Pharmacology: The Vascular System, 1999
    Co-Authors: Federico Dajas-bailador, Marcelo Asencio, Carolina Bonilla, Ma.cecilia Scorza, Carolina Echeverry, Miguel Reyes-parada, Rodolfo Silveira, P. Protais, Graeme Russell, Bruce K. Cassels

    Abstract:

    Abstract The dopaminergic and antioxidant properties of pukateine [(R)-11-hydroxy-1,2-methylenedioxyAporphine, PUK], a natural Aporphine Derivative, were analyzed in the rat central nervous system. At dopamine (DA) D1 ([3H]-SCH 23390) and D2 ([3H]-raclopride) binding sites, PUK showed IC50 values in the submicromolar range (0.4 and 0.6 μM, respectively). When the uptake of tritiated dopamine was assayed by using a synaptosomal preparation, PUK showed an IC50 = 46 μM. In 6-hydroxydopamine unilaterally denervated rats, PUK (8 mg/kg but not 4 mg/kg) elicited a significant contralateral circling, a behavior classically associated with a dopaminergic agonist action. When perfused through a microdialysis probe inserted into the striatum, PUK (340 μM) induced a significant increase in dopamine levels. In vitro experiments with a crude rat brain mitochondrial suspension showed that PUK did not affect monoamine oxidase activities, at concentrations as high as 100 μM. PUK potently IC 50 = 15 μM and dose-dependently inhibited the basal lipid peroxidation of a rat brain membrane preparation. As a whole, PUK showed a unique profile of action, comprising an increase in extracellular DA, an agonist-like interaction with DA receptors, and antioxidant activity. Thus, PUK may be taken as a lead compound for the development of novel therapeutic strategies for Parkinson disease.

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Che-ming Teng – One of the best experts on this subject based on the ideXlab platform.

  • Haemodynamic effects of dicentrine, a novel α1-adrenoceptor antagonist: Comparison with prazosin in spontaneously hypertensive and normotensive Wistar-Kyoto rats
    British Journal of Pharmacology, 1992
    Co-Authors: Shih‐yuan Hsu, Chien-chih Chen, Yu-ling Huang, Tur-fu Huang, Che-ming Teng

    Abstract:

    1
    The haemodynamic effects of dicentrine, an Aporphine Derivative isolated from the plant Lindera megaphylla, were investigated and compared with prazosin in rats.

    2
    In anaesthetized normotensive Wistar-Kyoto (WKY) rats, i.v. administration of dicentrine (0.1, 0.5, 1.0 mg kg−1) and prazosin (0.01, 0.05, 0.1 mg kg−1) induced a dose-related reduction of mean arterial pressure (MAP) which reached a maximal effect 5–10 min after injection and persisted for 2 h.

    3
    In anaesthetized WKY rats, a higher dose of dicentrine (1.0 mg kg−1, i.v.) did not cause any significant changes in heart rate (HR), cardiac output (CO) and stroke volume (SV) but markedly increased tail blood flow. In contrast, a higher dose of prazosin (0.1 mg kg−1, i.v.) produced a decrease in HR which paralleled the time course of the hypotensive response.

    4
    The hypotensive activity of dicentrine was completely abolished by α-adrenoceptor blockade. Both dicentrine and prazosin significantly attenuated pressor responses to noradrenaline but failed, even at maximal hypotensive doses, to impair the pressor effects of angiotensin II or vasopressin. These observations suggest that dicentrine appears to exert its hypotensive action through α1-adrenoceptor blockade.

    5
    In conscious normotensive and spontaneously hypertensive (SH) rats, dicentrine (0.5–2.0 mg kg−1, i.v.) and prazosin (0.05–0.2 mg kg−1, i.v.) also evoked dose-related decreases in MAP which were of greater magnitude in SH rats. Oral administration of dicentrine (5 and 8 mg kg−1) to conscious SH rats caused a hypotensive effect which persisted for over 15 h.

    6
    These results suggest that dicentrine may have therapeutic potential as an oral antihypertensive drug via α1-adrenoceptor blockade.

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