1 The selectivity of a number of agonists for peripheral alpha 1- and alpha 2- adrenoreceptors was determined and related to their cardiovascular effects in pentobarbitone-anaesthetized rats. 2 In isolated tissues, presynaptic alpha 2- and postsynaptic alpha 1-adrenoreceptor activity was determined on the rat vas deferens and anococcygeus muscle respectively. Xylazine, guanabenz, guanoxabenz and guanfacin were more selective, whilst lofexidine, tiamenidine, naphazoline, oxymetazoline and St 91 were less selective than clonidine for presynaptic alpha 2-adrenoreceptors. 3 The anococcygeus muscle of the pithed rat was used to determine the alpha-adrenoreceptor selectivity of the compounds in vivo. The selectivities were similar to those obtained in vitro. 4 Following intravenous administration to pentobarbitone-anaesthetized rats guanabenz and guanfacin caused small transient pressor responses and a prolonged secondary hypotension. In contrast oxymetazoline and St 91 produced marked initial pressor responses and the secondary reduction in blood pressure was absent. Clonidine and tiamenidine produced marked initial pressor responses followed by secondary hypotensive effects. All compounds reduced heart rate. 5 Intracerebroventricular (i.c.v.) administration of clonidine, guanabenz and guanfacin elicited falls in blood pressure and heart rate. In contrast blood pressure was either unaffected or elevated following i.c.v. administration of St 91, oxymetazoline and tiamenidine. 6 It is concluded that in the normotensive rat, central alpha 2-adrenoreceptors play a major role in the hypotensive effects of clonidine and related compounds.

I Intraventricular a-methyldopamine (50-200 gg) produced a dose-related fall in blood pressure in conscious spontaneously hypertensive rats. Pretreatment with intraventricular 6-hydroxydopamine prevented this hypotensive effect of a-methyldopamine. 2 The hypotensive effect of a-methyldopamine was prevented by intraventricular injection of phentolamine or desmethylimipramine, but not by intraperitoneal injection of haloperidol.3 Pretreatment with U-14,624, a selective central dopamine-4-hydroxylase inhibitor, prevented the hypotensive effect of a-methyldopamine. 4 cx-Methyldopamine was considerably less potent than noradrenaline as a pressor agent in the pithed rat, but noradrenaline and cx-methylnoradrenaline were found to be equipotent. 5 a-Methyldopamine (1-5 mg i.c.v.) reduced pressor responses elicited by electrical stimulation of the midbrain reticular formation in cats anaesthetized with chloralose. 6 It is concluded that the hypotensive action of ca-methyldopamine in conscious animals involves intact central ca-adrenergic neurones and a central adrenergic uptake mechanism for the formation of a-methylnoradrenaline.

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Salsolinol (Ia) wird ausgehend von 3,4‐Dihydro‐6,7‐dimethoxy‐1‐methyl‐isochinolin durch Reduktion mit Natriumborhydrid in Ethanol und anschließende Behandlung mit konz. HBr dargestellt.