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Arginine vasopressin, oxytocin and ACTH are released from the pituitary gland in response to acute hypoglycemia. To investigate the role of \g=a\-adrenergic mechanisms in mediating this response, 6 non-diabetic subjects were studied during hypoglycemia induced by 0.15 IU/kg iv insulin under control conditions, and during non-selective \g=a\-adrenergic blockade with phentolamine. In the control study plasma arginine vasopressin rose from 1.6\m=+-\0.8 pmol/l (mean \m=+-\sem) basally to a maximum of 2.5\m=+-\0.8 pmol/l following hypoglycemia (p<0.05). An exaggerated response was found during phentolamine blockade, with a maximum plasma vasopressin of 11.5\m=+-\0.4 pmol/l (by analysis of variance, p<0.05). The plasma oxytocin response to hypoglycemia was similarily increased during phentolamine compared to control. Plasma growth hormone rose to 94\m=+-\19mU/l, and during blockade with phentolamine the response was significantly reduced reaching a peak of 34\m=+-\7mU/l (by analysis of variance, p<0.05). ACTH and prolactin both increased in response to hypoglycemia, but the increases were not affected by phentolamine. An \g=a\-adrenergic mechanism appears to inhibit the release of arginine vasopressin and oxytocin in response to hypoglycemia, but does not appear to affect the secretion of ACTH.Acute insulin-induced hypoglycemia in normal humans provokes the rapid secretion of GH, ACTH, and PRL from the anterior pituitary gland, while oxytocin and AVP are released from the pos¬ terior pituitary gland (1,2). Although at present oxytocin and AVP are not regarded as major counterregulatory hormones, it is possible that they may have a minor role in glucose homeostasis, and con¬ tribute to the restoration of normoglycemia. Oxy¬ tocin and AVP in physiological doses stimulate the release of hepatic glucose and pancreatic glucagon in man (3,4). In pharmacological doses both hor¬ mones have been shown to increase glycogenolysis (5) and gluconeogenesis (6) in isolated rat hepatocytes. The release of oxytocin and AVP in re¬ sponse to hypoglycemia appears to occur indepen¬ dently of osmotic, hemodynamic and other factors which are involved in regulation of their seretion and is probably stimulated through a direct effect of neuroglycopenia on the hypothalamus (1,2), but the neurohumoral mechanisms involved are not well defined. It has been suggested that cCj adre¬ nergic receptors may be involved in inhibiting the release of AVP in response to hypoglycemia (7), but this assertion has been contradicted by others (8), and little is known about the role of these receptors in the release of oxytocin. The responses of AVP, oxytocin and ACTH during acute hypoglycemia were therefore examined in normal human sub¬ jects with and without non-selective a-adrenergic blockade using phentolamine to examine the in¬ volvement of putative adrenergic mechanisms. Subjects and MethodsApproval for this study was given by the local medical ethical advisory committee and informed consent was ob-

TIIE realizatioin that spasnm plays a part in a considerable proportion of the common) peripheral arterial diseases madle it necessary to develop methods for measuring it. The first attempts were niaturally concerneed more with the denmonstrationi that vasoconstriction was or was not present in any given case uln(ler stu(ly. These qualitative tests ha(l a definite place in emphasizing to the profession the importance of spasmn in the peripheral arterial (liseases.1, 2, 3, 4 The methods generally adopted to l)ring out the presence or absence of

No abstract