Jespersen B, Fogh-Andersen N, Brock A
Department of Medicine and Nephrology C, Skejby Hospital, Denmark.
Scand J Clin Lab Invest. 1994 Nov;54(7):531-41. doi: 10.3109/00365519409088565.
In order to elucidate a participation of intact parathyroid hormone (PTH(1-84)) in blood pressure (BP) and body fluid homeostasis, we studied fluctuations of PTH(1-84) during manipulations of BP in hyperparathyroid and healthy subjects, and during manipulations of blood volume in patients with glomerulonephritis or liver cirrhosis and in controls. Angiotensin II induced BP elevation was associated with increased values of PTH(1-84) both in healthy subjects (12-25 ng l-1, medians, p < 0.01), in patients with primary hyperparathyroidism (94-125 ng l-1, p < 0.01), in patients with low calcium due to end stage renal disease before requirement of dialysis (95-151 ng l-1, p < 0.02), and in patients with tertiary hyperparathyroidism (221-264 ng l-1, p < 0.05), but not in dialysis patients without hypercalcaemia (126-174 ng l-1, NS). The changes could not be attributed to reduction of serum calcium, but probably to the increase of plasma angiotensin II, which was positively correlated to the increase of serum PTH(1-84) in the healthy subjects (p = 0.619, n = 15, p < 0.05) and in the patients with primary hyperparathyroidism (p = 0.549, n = 18, p < 0.05). Noradrenaline induced BP elevation did not have a similar effect on PTH(1-84), and changes of PTH(1-84) were not related to changes of BP. Volume depletion after furosemide injection, also accompanied by increased levels of angiotensin II, resulted in elevation of PTH(1-84) in controls, cirrhotics, patients with glomerulonephritis without the nephrotic syndrome, but not in nephrotic patients. Volume depletion induced by bolus injection of atrial natriuretic peptide (ANP) was associated with decreased PTH(1-84) in healthy subjects (20-18 ng l-1, p < 0.02), but not in patients with nephrotic syndrome and liver cirrhosis. Volume expansion induced by albumin infusion caused increased plasma levels of ANP, but PTH(1-84) was unaltered. Thus, angiotensin II may be able to stimulate, and ANP to inhibit release of PTH(1-84), and PTH(1-84) may be involved in the regulation of BP and body fluid homeostasis. BP changes or changes in blood volume per se do not seem to influence PTH(1-84) levels.
为了阐明完整的甲状旁腺激素（PTH(1 - 84)）在血压（BP）和体液稳态中的作用，我们研究了甲状旁腺功能亢进患者和健康受试者在血压变化时，以及肾小球肾炎或肝硬化患者及其对照在血容量变化时PTH(1 - 84)的波动情况。在健康受试者（中位数为12 - 25 ng l-1，p < 0.01）、原发性甲状旁腺功能亢进患者（94 - 125 ng l-1，p < 0.01）、终末期肾病且未进行透析前低钙血症患者（95 - 151 ng l-1，p < 0.02）以及三发性甲状旁腺功能亢进患者（221 - 264 ng l-1，p < 0.05）中，血管紧张素II诱导的血压升高与PTH(1 - 84)值升高相关，但在无高钙血症的透析患者中（126 - 174 ng l-1，无显著性差异）无此现象。这些变化并非归因于血清钙的降低，而可能是由于血浆血管紧张素II的增加，这在健康受试者（p = 0.619，n = 15，p < 0.05）和原发性甲状旁腺功能亢进患者中（p = 0.549，n = 18，p < 0.05）与血清PTH(1 - 84)的增加呈正相关。去甲肾上腺素诱导的血压升高对PTH(1 - 84)没有类似影响，且PTH(1 - 84)的变化与血压变化无关。注射速尿后的容量耗竭，同样伴有血管紧张素II水平升高，导致对照组、肝硬化患者、无肾病综合征的肾小球肾炎患者的PTH(1 - 84)升高，但肾病患者无此现象。静脉推注心房利钠肽（ANP）引起的容量耗竭与健康受试者PTH(1 - 84)降低相关（20 - 18 ng l-1，p < 0.02），但肾病综合征和肝硬化患者无此现象。输注白蛋白引起的容量扩张导致血浆ANP水平升高，但PTH(1 - 84)未改变。因此，血管紧张素II可能能够刺激PTH(1 - 84)释放，而ANP则抑制其释放，且PTH(1 - 84)可能参与血压和体液稳态的调节。血压变化或血容量变化本身似乎并不影响PTH(1 - 84)水平。
