Young E W, Morris C D, Holcomb S, McMillan G, McCarron D A
Division of Nephrology, Hypertension, and Clinical Pharmacology, Oregon Health Sciences University, Portland, USA.
Am J Hypertens. 1995 Oct;8(10 Pt 1):957-64. doi: 10.1016/0895-7061(95)00214-6.
Patients with essential hypertension have been reported to have a higher serum concentration of parathyroid hormone (PTH) than normotensive individuals although this finding is not universal among studies. To further characterize the status of the calcium regulating hormones in essential hypertension, we measured the parathyroid gland response to acute EDTA-induced hypocalcemia and the renal response of 1,25(OH)2-vitamin D to dietary calcium deprivation in 16 hypertensive (H) and 15 normotensive (N) men. The average mean arterial blood pressure once all antihypertensive medications were discontinued was 108 +/- 7 mm Hg for the hypertensive group and 89 +/- 4 mm Hg for the normotensive group (P < .01). There were no group differences in baseline serum concentrations of ionized calcium, creatinine, intact PTH, and 1,25(OH)2-vitamin D, urinary calcium excretion, and creatinine clearance. After a 1-h infusion of EDTA at 12.5 mg/kg/h, the serum concentration of ionized calcium fell (H: 1.25 +/- .03 to 1.17 +/- .04 mmol/L, N: 1.26 +/- .04 to 1.18 +/- .04 mmol/L, P = NS) and PTH increased (H: 36 +/- 9 to 91 +/- 30 pg/mL, N: 40 +/- 14 to 85 +/- 28 pg/mL, P = NS). With an additional hour of EDTA at a dose of 25 mg/kg/h, serum ionized calcium concentration fell further (H: 1.01 +/- .05 mmol/L, N: 1.03 +/- .06 mmol/L, P = NS) and PTH increased to 150 +/- 58 pg/ml in patients and 130 +/- 32 pg/ml in controls (P < .001). The response suggested an increased maximal parathyroid gland secretory capacity in the hypertensive patients relative to the controls. There was no group difference in the serum concentration of 1,25(OH)2-vitamin D at baseline (H: 32 +/- 6 pg/ml, N: 32 +/- 8 pg/ml, P < .90) and following dietary calcium deprivation for three days (H 50 +/- 12, N 48 +/- 14 P < 0.76). The maximal stimulated PTH level was significantly higher in hypertensive than normotensive subjects in the absence of measured differences in serum ionized calcium concentration, serum 1,25(OH)2-vitamin D concentration, and creatinine clearance. These findings suggest an intrinsic alteration of PTH regulation in patients with essential hypertension, manifest as increased parathyroid gland secretory capacity.
据报道,原发性高血压患者的甲状旁腺激素(PTH)血清浓度高于血压正常者,不过这一发现并非在所有研究中都普遍存在。为了进一步明确原发性高血压患者钙调节激素的状态,我们测量了16名高血压男性(H组)和15名血压正常男性(N组)的甲状旁腺对急性乙二胺四乙酸(EDTA)诱导的低钙血症的反应,以及肾脏对饮食中钙缺乏时1,25(OH)₂ -维生素D的反应。在停用所有抗高血压药物后,高血压组的平均动脉血压为108±7 mmHg,血压正常组为89±4 mmHg(P < 0.01)。两组在基线时的血清离子钙、肌酐、完整PTH、1,25(OH)₂ -维生素D浓度、尿钙排泄和肌酐清除率方面没有差异。以12.5 mg/kg/h的速度输注EDTA 1小时后,血清离子钙浓度下降(H组:1.25±0.03至1.17±0.04 mmol/L,N组:1.26±0.04至1.18±0.04 mmol/L,P = 无显著性差异),PTH升高(H组:36±9至91±30 pg/mL,N组:40±14至85±28 pg/mL,P = 无显著性差异)。再以25 mg/kg/h的剂量额外输注1小时EDTA后,血清离子钙浓度进一步下降(H组:1.01±0.05 mmol/L,N组:1.03±0.06 mmol/L,P = 无显著性差异),患者的PTH升高至150±58 pg/ml,对照组为130±32 pg/ml(P < 0.001)。该反应表明高血压患者相对于对照组甲状旁腺的最大分泌能力增强。两组在基线时(H组:32±6 pg/ml,N组:32±8 pg/ml,P < 0.90)以及饮食中钙缺乏三天后(H组50±12,N组48±14,P < 0.76)的1,25(OH)₂ -维生素D血清浓度没有差异。在血清离子钙浓度、血清1,25(OH)₂ -维生素D浓度和肌酐清除率无测量差异的情况下,高血压患者的最大刺激PTH水平显著高于血压正常者。这些发现提示原发性高血压患者存在PTH调节的内在改变,表现为甲状旁腺分泌能力增强。