Mannelli M, Lanzillotti R, Pupilli C, Ianni L, Conti A, Serio M
Department of Clinical Physiopathology, University of Florence, Italy.
J Clin Endocrinol Metab. 1994 Jun;78(6):1331-5. doi: 10.1210/jcem.78.6.8200934.
To investigate whether chronic endogenous hypercortisolism might alter adrenomedullary phenylethanolamine N-methyltransferase activity, we measured epinephrine/norepinephrine (E/NE) ratios in the adrenal venous blood of 8 patients undergoing surgery for Cushing's syndrome and in 12 control subjects undergoing surgery for left kidney diseases. To investigate the adrenomedullary secretory activity in Cushing's syndrome, we measured basal E plasma levels in 24 patients and 32 age- and sex-matched normal control subjects, and we evaluated the adrenomedullary response to glucagon in 9 patients and in 22 age- and sex-matched normal subjects. Last, to clarify whether chronic endogenous hypercortisolism might modify E plasma levels through a modification of E metabolism, we measured the E MCR in four patients and four age-matched controls. Mean (+/- SEM) E/NE ratio in adrenal venous blood was similar in patients with Cushing's syndrome (4.61 +/- 0.78) and in the control group (4.71 +/- 0.74). Mean (+/- SEM) basal plasma E was significantly lower in patients with Cushing's syndrome (98.2 +/- 10.9 vs. 184 +/- 25.1 pmol/L, P < 0.01) than in the control group. Similarly, plasma NE also was reduced (0.75 +/- 0.09 vs. 1.10 +/- 0.07 nmol/L, P < 0.01). In patients with Cushing's syndrome the E response to glucagon was significantly reduced (P < 0.01). E MCR was almost identical in patients with Cushing's syndrome (1.48 +/- 0.10 L/min.m2) and in control subjects (1.51 +/- 0.10 L/min.m2). Our data demonstrate that: 1) chronic endogenous hypercortisolism is not able to change adrenomedullary phenylethanolamine N-methyltransferase activity and therefore the quality of adrenomedullary secretion; and 2) chronic endogenous hypercortisolism causes a decrease in basal and stimulated adrenomedullary activity without altering E MCR significantly. Therefore the adrenal medulla does not seem to play a pathogenetic role in the hypertension of Cushing's syndrome.
为了研究慢性内源性皮质醇增多症是否会改变肾上腺髓质苯乙醇胺N - 甲基转移酶的活性，我们测量了8例库欣综合征手术患者及12例左肾疾病手术对照者肾上腺静脉血中的肾上腺素/去甲肾上腺素（E/NE）比值。为了研究库欣综合征患者的肾上腺髓质分泌活性，我们测量了24例患者及32例年龄和性别匹配的正常对照者的基础血浆E水平，并评估了9例患者及22例年龄和性别匹配的正常受试者对胰高血糖素的肾上腺髓质反应。最后，为了阐明慢性内源性皮质醇增多症是否可能通过改变E代谢来改变血浆E水平，我们测量了4例患者及4例年龄匹配对照者的E清除率（MCR）。库欣综合征患者肾上腺静脉血中E/NE比值的均值（±标准误）（4.61±0.78）与对照组（4.71±0.74）相似。库欣综合征患者基础血浆E的均值（±标准误）（98.2±10.9对184±25.1 pmol/L，P<0.01）显著低于对照组。同样，血浆NE也降低（0.75±0.09对1.10±0.07 nmol/L，P<0.01）。库欣综合征患者对胰高血糖素的E反应显著降低（P<0.01）。库欣综合征患者的E MCR（1.48±0.10 L/min·m²）与对照者（1.51±0.10 L/min·m²）几乎相同。我们的数据表明：1）慢性内源性皮质醇增多症无法改变肾上腺髓质苯乙醇胺N - 甲基转移酶的活性，因此也无法改变肾上腺髓质分泌的质量；2）慢性内源性皮质醇增多症导致基础及刺激后的肾上腺髓质活性降低，但未显著改变E MCR。因此，肾上腺髓质似乎在库欣综合征高血压的发病机制中不起作用。
