Cerebral acting maps of hydralazine, clonidine, and .ALPHA.-methyldopa in spontaneously hypertensive rats as demonstrated by the 14C-deoxy-d-glucose method.

In spontaneously hypertensive rats, the 14C-deoxy-D-glucose method was applied to examine the response of glucose utilization rate (GUR), as a measure of the neuronal activity, of 102 cerebral nuclei to the equivalent fall in blood pressure by about 50 mmHg after the treatment with hydralazine, clonidine, and alpha-methyldopa. All drugs significantly increased GUR in the dorsal medullary nuclei, whereas the drugs decreased it in the n. tegmenti ventralis, substantia reticularis mesencephali, some hypothalamic periventricular nuclei, amygdala nuclei, and n. accumbens septi. Hydralazine (but not other drugs) decreased GUR in the n. parabrachialis ventralis, n. centromedianus, n. reticularis medialis and n. suprachiasmaticus. Clonidine alone increased GUR in medullary reticular nuclei and decreased it in the infundibulum, n. proprius striae terminalis and cortex entorhinalis. alpha-Methyldopa (but not other drugs) increased GUR in the n. reticularis parvocellularis and decreased it in the n. ambiguus, n. ventromedialis, area lateralis and anterior hypothalami, area preoptica medialis and n. medialis septi. Both clonidine and alpha-methyldopa (but not hydralazine) increased GUR in the n. reticularis thalami and decreased it in the substantia nigra pars compacta and grisea centralis, n. paramedianus, neuroendocrine hypothalamic nuclei, Forel H, and n. lateralis and intermedium septi. Clonidine and alpha-methyldopa did not alter GUR in some suprabulbar nuclei responsive to hydralazine. Thus, the non-traumatic deoxyglucose method could be applied successfully to identify cerebral acting sites of clonidine, alpha-methyldopa and hydralazine in SHR.