Physiological changes in directly recorded renal sympathoneural activity were related to changes in renal NE spillover into the bloodstream in rats, and physiological changes in skeletal muscle sympathoneural activity were related to changes in antecubital venous NE in humans. Juvenile spontaneously hypertensive rats had excessive sympathoadrenomedullary responsiveness to yohimbine without increases in corticotropin. About 1/3 of young patients with essential hypertension also had excessive sympathoadrenomedullary responsiveness to yohimbine with normal corticotropin responses. Young hypertensives had excessive sympathoadrenomedullary and pressor responses to playing a video game, with normal increments in mean arterial pressure for given increments in total body NE spillover. Patients with hypertrophic cardiomyopathy had defective neuronal uptake of NE. A method for in vivo measurement of reuptake of endogenously released NE was introduced, based on simultaneous measurements of NE and dihydroxyphenylglycol (DHPG). Regional release of dihydroxyphenylalanine (DOPA) indicated regional catecholamine biosynthesis. DOPA appeared to be a natriuretic neurohormone derived from sympathetic nerve endings and the brain. In dogs, all of urinary dopamine excretion was derived from plasma DOPA. Dietary salt loading increased urinary dopamine excretion by increasing DOPA delivery to renal uptake sites in humans. Salt- sensitive hypertensives appeared to have defective conversion of DOPA to dopamine in the kidney. Pituitary-adrenocortical and sympathoadrenomedullary system activities interacted in a compensatory manner to maintain homeostasis. PET scanning after injection of positron-emitting fluorodopamine successfully visualized tissue sympathetic innervation and function.
