Buzzeo L A, Steele J M, Lowenstein J
J Pharmacol Exp Ther. 1979 Nov;211(2):345-9.
We have examined insulin-induced hypoglycemia to determine whether prazosin inhibits the response to sympathetic stimulation, either centrally or at beta adrenergic receptors. Nine patients with essential hypertension were studied during administration of prazosin, hydralazine or placebo. Plasma renin activity increased significantly with hydralazine and was unchanged during prazosin administration. In response to insulin, blood glucose decreased equally with both drugs and placebo, and small increases in dopamine beta-hydroxylase occurred. Plasma renin activity and heart rate increased during hypoglycemia; the increases were greater in patients taking prazosin or hydralazine. The unimpaired responses of plasma dopamine beta-hydroxylase, renin activity and heart rate to insulin-induced hypoglycemia provide evidence that prazosin does not block either the sympathetic discharge elicited by central stimulation (hypoglycemia) or the responses mediated through beta adrenergic receptors.
我们研究了胰岛素诱导的低血糖,以确定哌唑嗪是否会抑制对交感神经刺激的反应,无论是在中枢还是在β肾上腺素能受体水平。在9例原发性高血压患者中,分别给予哌唑嗪、肼屈嗪或安慰剂进行研究。肼屈嗪给药后血浆肾素活性显著增加,而给予哌唑嗪期间血浆肾素活性无变化。对胰岛素的反应中,两种药物和安慰剂使血糖降低的程度相同,多巴胺β-羟化酶略有增加。低血糖期间血浆肾素活性和心率增加;服用哌唑嗪或肼屈嗪的患者增加幅度更大。血浆多巴胺β-羟化酶、肾素活性和心率对胰岛素诱导的低血糖反应未受损害,这表明哌唑嗪既不阻断中枢刺激(低血糖)引起的交感神经放电,也不阻断通过β肾上腺素能受体介导的反应。