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Division of Endocrinology, Diabetes, and Metabolism, General Clinical Research Center and the Diabetes Research and Training Center, Washington University School of Medicine, St. Louis, Missouri 63110
Plasma norepinephrine (NE) concentrations are a
fallible index of sympathetic neural activity because circulating NE
can be derived from sympathetic 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 FNESO, respectively) to study the sympathochromaffin
system during prolonged standing, hyperinsulinemic euglycemia, and
hyperinsulinemic hypoglycemia in healthy humans. Prolonged standing led
to decrements in blood 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 ml tissue
1), suggesting
that the approximately twofold increments in plasma NE and SNESO were
derived from sympathetic nerves other than those in the forearm (with a
possible contribution from the adrenal medullas). Hyperinsulinemia per
se (euglycemia maintained) stimulated sympathetic neural activity, as
evidenced by 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. Hypoglycemia 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 extent during hyperinsulinemic hypoglycemia than during
hyperinsulinemic euglycemia, FNESO was not. Thus these data do not
provide direct support for the concept that hypoglycemia per se also
stimulates sympathetic neural activity.
sympathetic nervous system; adrenal medullas; epinephrine; hypoglycemia
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