In dogs anesthetized with intravenous chloralose, vasopressin was injected either intravenously or into the cerebral ventricles, and the cardiovascular effects were studied before and after stabilizing the arterial blood pressure, bilateral vagotomy, and transection of the cervical cord at the level of C 2 . Intravenous vasopressin caused a rise in arterial blood pressure and pronounced bradycardia. The bradycardia appeared to be partly due to a peripheral depressant action on the heart, probably resulting from coronary constriction and partly from reflex vagal stimulation resulting from the rise in arterial blood pressure. A direct stimulating action of vasopressin on the central cardioinhibitory neurons played only a minor role in the production of the bradycardia. Injections of vasopressin, into either a lateral or the fourth ventricle, produced an insignificant rise in arterial blood pressure but marked bradycardia. A peripheral effect of the vasopressin after its absorption into the blood stream could be excluded as the cause of the bradycardia, since an injection of vasopressin into the cerebral ventricles produced diuresis, not antidiuresis. The bradycardia was more pronounced and occurred earlier when the vasopressin was injected into the fourth rather than into a lateral ventricle. The bradycardia produced by the injection of vasopressin into the cerebral ventricles could be almost fully accounted for by a central stimulating action on the cardioinhibitory neurons in the region of the vagal nuclei, which are closer to the fourth ventricle than to the lateral ventricles.From the

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Imipramine, a potent antidepressant, has been reported to cause hypotension in cats when administered intravenously.The fall in blood pressure due to high doses of imi pramine has been attributed to adrenergic blocking action of the drug (1). Lower doses of imipramine (320 ag/kg i.v.) also cause hypotension although at this dose level it does not produce adrenergic blockade. The cause of hypotension due to low doses of imipra mine has still not been explored and the reported observations do not provide any ex planation for this response. The ganglion blocking and the adrenergic neurone blocking action of imipramine has been ruled out by the observations of Osborne and Sigg (1).Furthermore, they have ruled out acetylcholine like action of imipramine. The direct vasodilator effect of this drug has been excluded (2). These reports exclude the possibility of action of small dose of imipramine on the efferent limb of the reflex arc regulating blood pressure. It was, therefore, thought desirable to study the effect of imipramine on the medullary and spinal vasomotor loci. MATERIAL AND METHODSThe study was carried out on 21 adult cats of either sex, anaesthetised with pento barbitone sodium (35 mg/kg i.p.). The animals were routinely vagotomised and main tained on artificial positive pressure respiration. The blood pressure was recorded from right common carotid artery through a mercury manometer on smoked kymograph paper. A femoral vein was cannulated for intravenous injections. A cannula was passed in a lateral cerebral ventricle according to the technique of Feldberg and Sherwood (3). The total volume of fluid injected at a time did not exceed 0.25 ml. The excitability of the medullary vasomotor center was assessed by : A) Direct electrical stimulation of the vasomotor center by an stereotaxically orient ed bipolar stainless steel electrode according to the parameters described by Wang and Ranson (4). B) Reflex stimulation of the vasomotor center by :