TREATMENT OF NEONATAL RATS WITH MONOSODIUM GLUTAMATE ATTENUATES THE CARDIOVASCULAR REACTIVITY TO PHENYLEPHRINE AND ANGIOTENSIN-II

In rats, neonatal administration of monosodium glutamate (MSG) causes serious damage in some hypothalamic and circumventricular areas. The r esulting loss of appropriate neurons important for the regulation of b lood pressure (BP) may modulate cardiovascular system receptivity in t hese animals. In the present study, the reactivity of the cardiovascul ar system to intravenous injection of alpha(1)-adrenergic receptor ago nist phenylephrine (200 mu g/kg/ml) and angiotensin II (500 ng/kg in 0 .6 ml for 2 min) was investigated in adult rats which had been neonata lly treated with MSG or vehicle. BP parameters measured directly in co nscious cannulated rats were continuously registered using a computeri zed system. Under basal conditions, MSG-treated rats had slightly lowe r systolic, diastolic and mean BP with significant differences in puls e pressure (systolic - diastolic BP). In MSG-treated animals, the maxi mal increase of mean arterial BP after phenylephrine and the duration of BP elevation after both agents were significantly reduced. Slopes o f the linear portion of baroreceptor function curves in control and MS G-treated rats did not differ significantly, indicating that barorefle x efficacy was unchanged. The results obtained by perfusion of the hin dlimb vascular bed in situ showed that the pressure responses to incre asing doses of noradrenaline in MSG-treated rats were reduced. These f indings demonstrate that neonatal treatment of rats with MSG lowers th e responsiveness of the cardiovascular system, particularly in respons e to alpha-adrenergic stimulation. It is suggested that the attenuatio n of cardiovascular reactivity in MSG-treated rats is, at least partly , caused by diminished vascular responsiveness.