Jespersen B, Randløv A, Abrahamsen J, Fogh-Andersen N, Kanstrup I L
Department of Medicine and Nephrology B, Herlev Hospital, University of Copenhagen, Denmark.
Am J Hypertens. 1997 Dec;10(12 Pt 1):1356-67. doi: 10.1016/s0895-7061(97)00275-6.
As it has been suggested that parathyroid hormone (PTH) is implicated in the pathophysiology of essential hypertension, the effects of PTH(1-34) were assessed during infusion over 120 min in ten men with essential hypertension and in ten healthy men. Ionized calcium was kept constant by a clamping technique. Mean arterial blood pressure fell slightly in the patients (116 mm Hg, median, before, and 108 mm Hg during the infusion, P < .01), but remained unchanged in the controls (median 87 mm Hg). The pulse rate rose to a similar extent in the two groups, but cardiac output, measured by the CO2 rebreathing technique, was unchanged. The glomerular filtration rate (GFR) was slightly lower in the hypertensives than in the controls at baseline (92 v 109 mL/min, P < .02), but it increased similarly during PTH infusion in both groups (+13% v +9%, medians), as did the effective renal plasma flow (+50% v +38%). The urinary rate of sodium excretion, which was similar at baseline, increased more in the patients than in the controls (+191% v +46%, P < .05); this was mainly attributable to a reduction in the tubular reabsorption of sodium. Calculations based on lithium clearance indicated that mainly the proximal tubular reabsorption of sodium decreased during PTH infusion. Baseline plasma PTH(1-84) was higher in the patients than in the controls (20.5 ng/L v 16.5 ng/L, P < .05). The baseline plasma values of renin, aldosterone, atrial natriuretic peptide, endothelin, and noradrenaline were similar in the two groups. During infusion of PTH, renin increased less in the patients than in the controls (P < .02), and aldosterone increased only in the controls (P < .01). The other hormonal values remained unchanged. In conclusion, the patients with essential hypertension had increased baseline PTH values, but nevertheless PTH had more marked vasodilative and natriuretic effects than in the controls. PTH thus seems to counteract rather than aggravate elevation of blood pressure in these patients.
由于有人提出甲状旁腺激素（PTH）与原发性高血压的病理生理机制有关，因此对10名原发性高血压男性患者和10名健康男性在120分钟内静脉输注PTH（1 - 34）期间的效果进行了评估。采用钳夹技术使离子钙保持恒定。患者的平均动脉血压略有下降（中位数，输注前为116 mmHg，输注期间为108 mmHg，P < 0.01），但对照组未发生变化（中位数87 mmHg）。两组的脉搏率上升幅度相似，但通过二氧化碳重呼吸技术测量的心输出量未发生变化。高血压患者的肾小球滤过率（GFR）在基线时略低于对照组（92对109 mL/分钟，P < 0.02），但两组在PTH输注期间均有相似程度的增加（中位数分别增加13%对9%），有效肾血浆流量也是如此（分别增加50%对38%）。基线时相似的尿钠排泄率在患者中增加幅度大于对照组（分别增加191%对46%，P < 0.05）；这主要归因于肾小管对钠的重吸收减少。基于锂清除率的计算表明，在PTH输注期间主要是近端肾小管对钠的重吸收减少。患者的基线血浆PTH（1 - 84）高于对照组（20.5 ng/L对16.5 ng/L，P < 0.05）。两组的肾素、醛固酮、心房利钠肽、内皮素和去甲肾上腺素的基线血浆值相似。在输注PTH期间，患者肾素的增加幅度小于对照组（P < 0.02），醛固酮仅在对照组中增加（P < 0.01）。其他激素值保持不变。总之，原发性高血压患者的基线PTH值升高，但尽管如此，PTH在这些患者中具有比对照组更明显的血管舒张和利钠作用。因此，PTH似乎在这些患者中起到抵消而非加重血压升高的作用。
