Abstract
The extensive destruction of forebrain noradrenergic nerve terminals by the intraventricular injection of 250 micrograms of 6-hydroxydopamine prevents the subsequent development of DOCA-salt experimental hypertension in rats while the lesser destruction of noradrenergic nerve terminals produced by 90 micrograms of 6-hydroxydopa does not. The greatest difference in brain part noradrenaline levels between these two neurotoxins was in the septal area where noradrenaline was less than 15% of controls after 6-hydroxydopamine but was the same as controls after 6-hydroxydopa. The non-specific destruction of the lateral septal area by radiofrequency lesions prevented the subsequent development of DOCA-salt hypertension. The relatively selective destruction of catecholamine nerve terminals in the lateral septal area by the injection of 1 microgram 6-hydroxydopamine in 1 microliter vehicle also prevented the development of DOCA-salt hypertension. These data suggest that the lateral septal area may be the location of the forebrain catecholaminergic neural activity that is necessary for the development of DOCA-salt experimental hypertension in rats.
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