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Cardiovascular effects of 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride (ST 115)

1968; Elsevier BV; Volume: 2; Issue: 5 Linguagem: Inglês

10.1016/0014-2999(68)90184-2

1879-0712

H Schmitt, Mme Hélène Schmitt, J.R. Boissier, J. F. Giudicelli, J. Fichelle,

Receptor Mechanisms and Signaling

In order to discover whether 2-(2,6-dichlorophenylamino)-2-imidazoline hydrochloride (ST 155) has a central site of action, the influence of the drug on spontaneous discharges of sympathetic nerves, and on evoked discharges elicited by chemostimulant drugs or electrical stimulation of sympathetic structures of the brain stem was investigated. In dogs, ST 155 induced bradycardia and hypertension which was usually followed by hypotension. Discharges in splanchnic and inferior cardiac nerves were strikingly reduced or even abolished by ST 155, recovery appearing sometimes after three hours. The site of action appeared to be central because the phenomenon was also observed in debuffered dogs. However, activity in sympathetic nerves could still be evoked by chemo receptor stimulating drugs. Injected intracisternally, ST 155 induced a decrease in blood pressure and a reduction in sympathetic discharges. In cats, the same reduction of spontaneous electrical activity of sympathetic nerves was observed. In addition, increase in blood pressure and evoked discharges induced by hypothalamic and medullary pressor areas stimulation were decreased, but the effects of supramaximal stimulation were not modified. In rats, action potentials in the splanchnic nerve, as well as the evoked discharges elicited by hypothalamic and medullary stimulations were reduced by ST 155. ST 155 appears to be a very potent inhibitor of the spontaneous sympathetic centre in the brain stem, but is less effective on reflexly or centrally evoked discharges.