Abrahm D R, Hollingsworth P J, Smith C B, Jim L, Zucker L B, Sobotka P A, Vinik A I
J Clin Endocrinol Metab. 1986 Oct;63(4):906-12. doi: 10.1210/jcem-63-4-906.
Platelet adrenergic receptors were studied in normal subjects and diabetic patients with autonomic neuropathy to determine the relationship between adrenoreceptor status and orthostatic hypotension. The binding of [3H]clonidine and [3H]yohimbine to platelet membranes was measured in diabetic patients with autonomic neuropathy and orthostatic hypotension (n = 12) and without orthostatic hypotension (n = 11), diabetic patients without autonomic neuropathy (n = 12), and normal subjects (n = 9). Mean basal and standing plasma norepinephrine levels were not different in the four groups, and there was no relationship between orthostasis and norepinephrine responses. The diabetic patients with orthostatic hypotension had a significantly greater fall in mean blood pressure [31 +/- 2.8 (+/- SE) mm Hg] than any of the other three groups. Diabetic patients with diabetic autonomic neuropathy and orthostatic hypotension had a 30-40% decrease in number of platelet alpha 2-adrenergic receptors, as demonstrated by [3H]clonidine and [3H]yohimbine binding. The maximum number of binding sites for clonidine was 34 +/- 2.8 (+/- SE) fmol/mg protein in normal subjects, 27.4 +/- 3.4 in diabetic patients with neuropathy, 26 +/- 2.5 in diabetic patients with autonomic neuropathy without orthostatic hypotension, and 20.4 +/- 3.8 fmol/mg protein in diabetic patients with autonomic neuropathy with orthostatic hypotension (P less than 0.001). The maximum number of binding sites for yohimbine was 112 +/- 12.6 in normal subjects, 127 +/- 10 in diabetic patients without orthostatic hypotension, and 87 +/- 12.4 fmol/mg protein in patients with diabetic autonomic neuropathy with orthostatic hypotension (P less than 0.001). Reduced platelet alpha 2-receptors are associated with postural hypotension in diabetic autonomic neuropathy. If applicable to the postjunctional alpha 2-adrenergic receptor on sympathetic neurons, reduced vascular responses to changes in posture would be expected despite normal or enhanced norepinephrine secretion.
对正常受试者和患有自主神经病变的糖尿病患者的血小板肾上腺素能受体进行了研究，以确定肾上腺素能受体状态与体位性低血压之间的关系。在患有自主神经病变和体位性低血压的糖尿病患者（n = 12）、无体位性低血压的糖尿病患者（n = 11）、无自主神经病变的糖尿病患者（n = 12）以及正常受试者（n = 9）中，测量了[3H]可乐定和[3H]育亨宾与血小板膜的结合情况。四组患者的平均基础和站立时血浆去甲肾上腺素水平无差异，体位改变与去甲肾上腺素反应之间也无关联。患有体位性低血压的糖尿病患者平均血压下降幅度[31±2.8（±标准误）mmHg]明显大于其他三组中的任何一组。通过[3H]可乐定和[3H]育亨宾结合实验表明，患有糖尿病自主神经病变和体位性低血压的患者血小板α2 - 肾上腺素能受体数量减少了30% - 40%。可乐定结合位点的最大数量在正常受试者中为34±2.8（±标准误）fmol/mg蛋白质，在患有神经病变的糖尿病患者中为27.4±3.4，在无体位性低血压的自主神经病变糖尿病患者中为26±2.5，在患有体位性低血压的自主神经病变糖尿病患者中为20.4±3.8 fmol/mg蛋白质（P < 0.001）。育亨宾结合位点的最大数量在正常受试者中为112±12.6，在无体位性低血压的糖尿病患者中为127±10，在患有体位性低血压的糖尿病自主神经病变患者中为87±12.4 fmol/mg蛋白质（P < 0.001）。血小板α2受体减少与糖尿病自主神经病变中的体位性低血压有关。如果这适用于交感神经元上的节后α2 - 肾上腺素能受体，那么尽管去甲肾上腺素分泌正常或增加，预计血管对体位变化的反应仍会降低。
