Stimultaion of
cyclic AMP formation by
epinephrine and
norepinephrine has been studied in discrete areas of rat brain that include the
epinephrine-containing brain stem nuclei C-1 and C-2. In the C-1 area,
epinephrine-stimulated
cyclic AMP formation was partially reversed by 100 microM
phentolamine and by 10--100 microM
propranolol or
alprenolol and hence appeared to involve activation of a mixture of both alpha- and
beta-adrenergic receptors as has been reported for other rat brain areas such as the cerebral cortex. However, in the C-2-area, the
epinephrine and
norepinephrine stimulated
cyclic AMP formation involved the activation of a single receptor type which was alpha-like in character. Stimulation of
cyclic AMP formation by
epinephrine in the C-2 area was antagonized by nanomolar concentrations of both
phentolamine and
yohimbine. The
epinephrine-stimulated formation of
cyclic AMP in the C-2 but not in the C-1 area was augmented in a strains of rats which exhibit spontaneous genetic
hypertension (SHR) vs. Wistar-Kyoto controls. It is suggested that the enhanced
epinephrine-stimulated
cyclic AMP formation in the C-2 area of SHR rats could be a physiological compensatory response to some other
hypertension-causing lesion which, for example, results in chronically reduced
epinephrine release or in ruduced availability of
epinephrine at its postsynaptic receptor thereby leading to receptor supersensitivity. Supporting this possibility was the finding that treatment of SHRs and control animals and
reserpine resulted in enhancement of
epinephrine-stimulated
cyclic AMP formation in the C-2 area of control rats, essentially obliterating the difference between control and SHR. The findings are also interepreted as supporting the involvement of
epinephrine neurons in central vaso-depressor mechanisms.