Lowder S C, Hamet P, Liddle G W
Circ Res. 1976 Feb;38(2):105-8. doi: 10.1161/01.res.38.2.105.
Insulin-induced hypoglycemia previously has been shown to provoke a beta-adrenergic response that normally results in an increase in plasma renin activity (PRA). In our study, hypoglycemia induced definite increases in PRA in a group of five patients with normal renin essential hypertension but failed to do so in a group of six patients with low renin essential hypertension. In both groups, plasma cyclic adenosine 3',5'-monophosphate (cyclic AMP; cAMP) increased more than 2-fold during hypoglycemia, but the response in the low renin group was significantly less than that previously observed in normal subjects under the same conditions. Plasma cortisol increased to an equal extent in both groups of hypertensive patients during hypoglycemia. Infusion of the phosphodiesterase inhibitor, theophylline, resulted in definite increases of PRA in patients with normal renin hypertension but not in patients with low renin hypertension. Because changes in the level of plasma cAMP during hypoglycemia have been thought to reflect adrenal catecholamine release, our finding of a blunted increase in plasma cAMP during hypoglycemia in patients with low renin hypertension may suggest that there is a generalized alteration in adrenergic responsiveness in this condition.
胰岛素诱导的低血糖症此前已被证明会引发β-肾上腺素能反应,这种反应通常会导致血浆肾素活性(PRA)升高。在我们的研究中,低血糖症在一组五名肾素正常的原发性高血压患者中导致PRA明显升高,但在一组六名肾素低的原发性高血压患者中却未出现这种情况。在两组患者中,低血糖期间血浆环磷酸腺苷(cAMP)均增加了两倍以上,但肾素低的组的反应明显低于之前在相同条件下正常受试者中观察到的反应。低血糖期间,两组高血压患者的血浆皮质醇升高程度相同。输注磷酸二酯酶抑制剂茶碱可使肾素正常的高血压患者的PRA明显升高,但肾素低的高血压患者则无此现象。由于低血糖期间血浆cAMP水平的变化被认为反映了肾上腺儿茶酚胺的释放,我们发现在肾素低的高血压患者中,低血糖期间血浆cAMP升高不明显,这可能表明在这种情况下肾上腺素能反应存在普遍改变。