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Am J Physiol Regul Integr Comp Physiol (January 15, 2004). doi:10.1152/ajpregu.00254.2002
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Submitted on May 6, 2002
Accepted on January 9, 2004

Dissociation of hypothalamic noradrenergic activity and sympathoadrenal responses to recurrent hypoglycemia

Martin G De Vries1, Marcus A Lawson2, and J. Lee Beverly1*

1 Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA; Neuroscience Program, University of Illinois at Urbana-Champaign, Urbana, IL, USA
2 Animal Sciences, University of Illinois at Urbana-Champaign, Urbana, IL, USA

* To whom correspondence should be addressed. E-mail: beverly1{at}uiuc.edu.

This study evaluated whether attenuation of sympathoadrenal responses to recurrent hypoglycemia is mediated by diminished noradrenergic activity in the hypothalamus. Male Sprague-Dawley rats received either once-daily insulin (1.0 units/kg) injections, or an equal administration of saline for three days. Both groups received an administration of insulin on the fourth day, during which blood glucose, and plasma catecholamines were determined, and extracellular norepinephrine (NE) in the ventromedial hypothalamus (VMH) or paraventricular hypothalamic nucleus (PVN) was monitored with microdialysis. The peak response of plasma epinephrine to insulin-induced hypoglycemia (nadir ~ 3.2 mmol/l) was significantly reduced during the fourth hypoglycemic episode (774 ± 134 pg/ml) as compared with the first episode (2561 ± 410 pg/ml, p < 0.001). Baseline levels of extracellular NE were elevated ~ 25% (p=0.07) in the VMH and ~46% (p=0.03) in the PVN after multiple hypoglycemic episodes. There was no difference in noradrenergic activity during the first or fourth hypoglycemic episode in either brain area. The reduced sympathoadrenal output after recurrent hypoglycemia is likely postsynaptic from hypothalamic NE release or is mediated via a collateral pathway.




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