FOREARM NOREPINEPHRINE SPILLOVER DURING STANDING, HYPERINSULINEMIA, AND HYPOGLYCEMIA

Plasma norepinephrine (NE) concentrations are a fallible index of symp athetic neural activity because circulating NE can be derived from sym pathetic nerves, the adrenal medullas, or both and because of regional differences in sympathetic neural activity, We used isotope dilution measurements of systemic and forearm NE spillover rates (SNESO and FNE SO, respectively) to study the sympathochromaffin system during prolon ged standing, hyperinsulinemic euglycemia, and hyperinsulinemic hypogl ycemia in healthy humans. Prolonged standing led to decrements in bloo d pressure without increments in heart rate, the pattern of incipient vasodepressor syncope. FNESO was not increased (0.58 +/- 0.20 to 0.50 +/- 0.21 pmol . min(-1). 100 mi tissue(-1)), suggesting that the appro ximately twofold increments in plasma NE and SNESO were derived from s ympathetic nerves other than those in the forearm (with a possible con tribution from the adrenal medullas). Hyperinsulinemia per se (euglyce mia maintained) stimulated sympathetic neural activity, as evidenced b y increments in FNESO (0.57 +/- 0.11 to 1.25 +/- 0.25 pmol . min(-1). 100 ml tissue(-1), P < 0.05), but not adrenomedullary activity. Hypogl ycemia per se stimulated adrenomedullary activity (plasma epinephrine from 190 +/- 70 to 1720 +/- 320, pmol/l, P < 0.01). Although SNESO (P < 0.05) and perhaps plasma NE (P < 0.06) were raised to a greater exte nt during hyperinsulinemic hypoglycemia than during hyperinsulinemic e uglycemia, FNESO was not. Thus these data do not provide direct suppor t for the concept that hypoglycemia per se also stimulates sympathetic neural activity.