Insulin-induced hypoglycemia induced a fall in blood pressure (BP) in patients with idiopathic orthostatic hypotension (IOH) and multiple system atrophy (MSA), but not in control subjects. Only in IOH was there a correlation between plasma norepinephrine (NE) levels and maintenance of BP during the test. The hypotension was not affected by pretreatment with propranolol. Hypotension during insulin-induced hypoglycemia is manifested in patients who lack an adequate NE response. The hypotension, however, may be due to a central action of insulin because not all MSA patients with impaired NE release become hypotensive.
Plasma epinephrine (EPI), norepinephrine (NE), beta-endorphin, and corticotropin (ACTH) responses were measured during insulin-induced hypoglycemia in normal subjects and in patients with either multiple system atrophy (MSA) or idiopathic orthostatic hypotension (IOH). In normal subjects, there was a striking rise in EPI, NE, beta-endorphin, and ACTH following the nadir of hypoglycemia. Both beta-endorphin and ACTH responses were significantly lower than normal in patients with MSA, in contrast to normal levels in IOH patients. No correlation was observed between the degree of adrenergic insufficiency and the beta-endorphin and ACTH responses. The normal peptide responses in IOH are consistent with involvement limited to the peripheral sympathetic nervous system, whereas lesions in the central nervous system in MSA interfere with release of beta-endorphin and ACTH in response to hypoglycemia. The strong correlation between beta-endorphin and ACTH levels is consistent with their common origin. Peripheral adrenergic activity is not essential for beta-endorphin and ACTH release in humans.
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