ABSTRACT
The most striking finding obtained from studies of depressed subjects, both hypersympathetic and hyposympathetic, is the observation that clonidine, besides its well-known ability to modify plasma growth hormone concentrations in depressed subjects, is likewise unable to modify these subject’s plasma coortisol (CRT) concentrations, although the drug did alter plasma CRT in normals. The administration of clonidine provoked a strikingly greater reduction of diastolic blood pressure, noradrenergic, and CRT during the exacerbation periods than during the nonexacerbation periods, and also compared to normals. A clonidine-induced reduction of norepinephrine release at the posterior hypothalamic level, along with a clonidine-induced increase of norepinephrine release at the anterior hypothalamic level, as postulated herein, is consistent with the findings that microinjection of norepinephrine in the posterior hypothalamus increases blood pressure and peripheral sympathetic activity, while norepinephrine microinjection in the anterior hypothalamus decreases blood pressure and peripheral sympathetic activity.
