Tetrahydroalstonine
Tetrahydroalstonine and Raubasine preferentially block the pressor responses of post-synaptic alpha-adrenergic receptor activation due to exogenous and endogenouse noradrenaline, respectively.
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J Pharmacol. 1985 Oct-Dec;16(4):412-20.
Differential inhibition of raubasine and tetrahydroalstonine on the vasopressor response to sympathetic nervous stimulation and intravenous noradrenaline in the pithed rat[Pubmed:
2869187]
The effects of raubasine and Tetrahydroalstonine (THA) on the vasopressor response to sympathetic nerve stimulation and to i.v. administration of noradrenaline were studied in the pithed rat to ascertain whether raubasine and THA would preferentially block pressor responses due to exogenous versus endogenous noradrenaline alpha-adrenergic receptor activation.
METHODS AND RESULTS:
Raubasine (0.5 to 4 mg/kg i.v.) was more effective in blocking the response due to sympathetic nerve stimulation than that due to i.v. noradrenaline. On the other hand THA (0.5 to 4 mg/kg i.v.) produced greater inhibition of the i.v. noradrenaline response than the sympathetic nerve stimulation response. THA (0.5, 1, 2 mg/kg i.v.) enhanced the nerve stimulation response, while at the 4 mg/kg dose the response was slightly reduced. This may be explained by a preferential block by THA at low doses, of presynaptic alpha 2-adrenoceptors. In pithed rat raubasine and THA showed dose-related blocking effects on the pressor response of phenylephrine and B-HT 933, respectively. This suggest that raubasine preferentially blocks alpha-1 and THA alpha 2-adrenoceptors.
CONCLUSIONS:
The results suggest that raubasine and THA preferentially block the pressor responses of post-synaptic alpha-adrenergic receptor activation due to endogenous and exogenous noradrenaline, respectively.
Eur J Pharmacol. 1984 Oct 30;106(1):203-5.
Inhibition of the alpha 1 and alpha 2-adrenoceptor-mediated pressor response in pithed rats by raubasine, tetrahydroalstonine and akuammigine.[Pubmed:
6099269]
METHODS AND RESULTS:
The relative potencies of raubasine, Tetrahydroalstonine (THA) and akuammigine on alpha 1- and alpha 2-adrenoceptors were assessed by comparing their effects on the rise in blood pressure induced by stimulation of the sympathetic outflow from the spinal cord or by injection of noradrenaline in pithed rats. Akuammigine was inactive in both cases. Raubasine preferentially antagonized the effects of electrical stimulation while Tetrahydroalstonine antagonized the effects of injected noradrenaline.
CONCLUSIONS:
The results suggest that raubasine preferentially blocks alpha 1-adrenoceptors while Tetrahydroalstonine is more selective for alpha 2-adrenoceptors.
