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Effects of clonidine on hormone and substrate responses to hypoglycemia
Author(s) -
Metz Stewart A,
Halter Jeffrey B
Publication year - 1980
Publication title -
clinical pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.941
H-Index - 188
eISSN - 1532-6535
pISSN - 0009-9236
DOI - 10.1038/clpt.1980.186
Subject(s) - hypoglycemia , endocrinology , basal (medicine) , clonidine , medicine , glucagon , insulin , catecholamine , biology
We have reported that clonidine (CLON) reduces basal norepinephrine (NE) levels but has no effect on basal epinephrine (E) levels. To study the effects of CLON on stimulated NE and E secretion, six normal men received a single dose of CLON followed by induction of hypoglycemia with insulin. Despite the presence of a mean hypoglycemic nadir of 44 mg/100 ml, there was no rise in E and NE levels during CLON treatment. To determine the effects of such catecholamine inhibition on the counterregulation of hypoglycemia, additional experiments were performed since the mean glucose nadir during CLON in the initial studies was slightly (9 mg/100 ml) less deep than in controls. When subjects on CLON received higher doses of insulin, glucose responses were identical to control responses; CLON still reduced the 0 to 60‐min catecholamine response by 83% (p < 0.02). Glucagon secretion was not impaired, but CLON blunted the early rate of glucose recovery in the first 15 min after the glucose nadir. We conclude that CLON inhibits the catecholamine (but not the glucagon) rise during insulin‐induced hypoglycemia. Selective inhibition of catecholamine secretion does not inhibit the glucogan response but leads to definite, although transient, inhibition of glucose recovery after hypoglycemia. Clinical Pharmacology and Therapeutics (1980) 28, 441–448; doi: 10.1038/clpt.1980.186