?-Sympathicomimetische Eigenschaften als Ursache der blutdrucksteigernden und blutdrucksenkenden Wirkung von BAY 1470 (2-(2,6-Xylidino)-5,6-dihydro-4H-1,3-thiazinhydrochlorid)

Abstract

1. Phentolamine antagonizes the pressor response as well as the response of the nictitating membrane of the cat to BAY 1470. After propranolol the pressor response to BAY 1470 is unchanged while that to adrenaline is increased. 2. In concentrations of up to 10−3 g/ml BAY 1470 is devoid of any activity on isolated guinea-pig atria; hence, BAY 1470 does not seem to act onβ-receptors. 3. BAY 1470 has noindirect sympathomimetic effects. Cocaine antagonizes the pressor effect of tyramine but not that of BAY 1470. Pretreatment with reserpine does not reduce the pressor response to BAY 1470. The output of noradrenaline from the spleen does not increase during perfusion with BAY 1470. 4. The initial pressor response to BAY 1470 is followed by a prolonged fall in blood pressure; the latter seems to be due to an inhibition of the release of noradrenaline from the peripheral sympathetic neurones as well as to a central site of action. The peripheral site of action could be demonstrated by a diminished output of noradrenaline from the splenic nerves following electrical stimulation during perfusion with BAY 1470. The central origin of the depressor response has been demonstrated by its occurence during perfusion of the fourth ventricle with BAY 1470. 5. As the depressor response following the ventricular perfusion with BAY 1470 is inhibited by phentolamine and dibenzyline perfusion of the ventricle, the central depressor action seems to be mediated byα-receptors located in the vicinity of the fourth ventricle.