LETTER
Prazosin, Diuretics, and Glucose Intolerance
Ivan Berlin
15 October 1993 | Volume 119 Issue 8 | Pages 859-860
TO THE EDITOR:
In their recent review of drug-induced disorders of glucose tolerance, Pandit and colleagues [1] state that prazosin, an 
-1-adrenoceptor antagonist, may improve glucose tolerance through increased glucose-dependent insulin secretion. They suggest that this effect results from decreased -2-adrenoceptor stimulation [2].
However, Broadstone and colleagues [2] tested phentolamine, an -1-adrenoceptor and -2-adrenoceptor antagonist, and found that this agent improved glucose-potentiated insulin secretion in patients with non-insulin-dependent diabetes mellitus. Because -adrenoceptors on pancreatic ß-cells are of the -2 subtype [3], this effect of phentolamine can only be attributed to an -2-adrenoceptor and not -1-adrenoceptor blockade. To our knowledge, there is no clinical evidence that prazosin improves glucose tolerance. However, if prazosin and other -1-adrenoceptor antagonists do improve glucose tolerance, it is possibly by increasing peripheral glucose uptake through raised muscle blood flow [4].
1. Pandit MK, Burke J, Gustafson AB, Minocha A, Peiris AN. Drug-induced disorders of glucose tolerance. Ann Intern Med. 1993; 118: 529-39.
2. Broadstone VI, Pfeifer MA, Bajaj V, Stagner JI, Samols E. Alpha-adrenergic blockade improves glucose-potentiated insulin secretion in non-insulin-dependent diabetes mellitus. Diabetes. 1987; 36:932-7.
3. Nakadate T, Nakaki T, Muraki T, Kato R. Adrenergic regulation of blood glucose levels: possible involvement of postsynaptic -2 type adrenergic receptors regulating insulin release. J Pharmacol Exp Ther. 1980; 215:226-30.
4. Baron AD. Vascular tone and insulin sensitivity: a potential role for blockade. Seventh Scientific Meeting of the American Society of Hypertension. Symposium: Sympathetic activation, blockade, and cardiovascular risk factors: putting the pieces together. New York; 6 May 1992.
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