6-hydroxydopamine destruction of central adrenergic neurones prevents or reverses developing DOCA-salt hypertension in rats.
The role of brain catecholaminergic neurones in the pathogenesis of DOCA-salt hypertension in the rat was investigated by selective depletion of central catecholamines using intraventricular or intracisternal administration of 6-hydroxydopamine (6-OHDA). Only the intraventricular injections prevented the development of hypertension. In addition, intraventricular 6-OHDA reversed the hypertension produced by two weeks but not six weeks of DOCA-salt treatment. The ability of intraventricular injections of 6-OHDA to prevent or reverse DOCA-salt hypertension while intracisternal injections do not, appears to be related to the greater depletion of brain catecholamines produced by the intraventricular injections. Only in the spinal cord and in the locus coeruleus were the norepinephrine contents depleted equally by either injection route. These findings suggest that central catecholaminergic neurones other than those originating in the locus coeruleus or descending in the spinal cord are important in the initiation, but not in the long term maintenance, of DOCA-salt hypertension. The influence of the central catecholamine neurons involved in the development of DOCA-salt hypertension might be mediated neurally via nonadrenergic pathways or hormonally via the brain-pituitary-endocrine system.
D000320:Adrenergic Fibers / Q000503:physiopathology; D000818:Animals; D001921:Brain / Q000378:metabolism; D002490:Central Nervous System / Q000503:physiopathology*; D003900:Desoxycorticosterone; D006892:Hydroxydopamines; D006973:Hypertension / Q000139:chemically induced* / Q000503:physiopathology; D008297:Male; D009638:Norepinephrine / Q000378:metabolism; D051381:Rats; D012965:Sodium Chloride
D006892:Hydroxydopamines; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D009638:Norepinephrine