Ueno H, Takata M, Oh-hashi S, Tomoda F, Yasumoto K, Iida H, Sasayama S
Second Department of Internal Medicine, Toyama Medical and Pharmaceutical University, Japan.
J Hum Hypertens. 1993 Apr;7(2):125-30.
We investigated the effect of one year of enalapril monotherapy on vascular structural changes and calcium metabolism in ten patients with essential hypertension. BP decreased from 169-10/103 +/- 10 mmHg during the placebo period to 138-12/82 +/- 10 mmHg after enalapril therapy. Minimal vascular resistance assessed by the venous occlusion technique with strain-gauge plethysmography was higher in the hypertensive patients than in the normotensive subjects (2.7 +/- 1.2 vs. 1.2 +/- 0.3 mmHg/ml/min per 100 ml tissue, P < 0.01). Although the elevated minimal vascular resistance seen in essential hypertensives decreased to 1.7 +/- 0.5 mmHg/ml/min per 100 ml tissue after enalapril (P < 0.01), it remained higher than that of normotensives (P < 0.05). Cytosolic free calcium ([Ca2+]i) in platelets measured by a Qiun-2 fluorescent indicator was higher in essential hypertensives than in normotensives (189 +/- 38 nM and 138 +/- 14 nM, respectively; P < 0.01). [Ca2+]i of essential hypertensives was reduced to 138 +/- 19 nM after treatment. Plasma renin activity was significantly increased after enalapril. Although plasma ionized calcium concentration did not change, parathyroid hormone was significantly increased after enalapril (from 0.36 +/- 0.22 to 0.58-0.32 ng/ml, P < 0.05). During the placebo period, minimal vascular resistance was correlated with [Ca2+]i (r = 0.62, P < 0.01). There was a close relationship between the changes in minimal vascular resistance and [Ca2+]i (r = 0.78, P < 0.01); however the change in minimal vascular resistance was not associated with changes in BP, catecholamine or parathyroid hormone.(ABSTRACT TRUNCATED AT 250 WORDS)
我们研究了依那普利单药治疗一年对10例原发性高血压患者血管结构变化和钙代谢的影响。血压在安慰剂期为169/103±10 mmHg，依那普利治疗后降至138/82±10 mmHg。采用应变片体积描记法的静脉闭塞技术评估的最小血管阻力，高血压患者高于血压正常者（每100 ml组织2.7±1.2 vs. 1.2±0.3 mmHg/ml/min，P<0.01）。虽然原发性高血压患者升高的最小血管阻力在依那普利治疗后降至每100 ml组织1.7±0.5 mmHg/ml/min（P<0.01），但仍高于血压正常者（P<0.05）。用喹啉-2荧光指示剂测量的原发性高血压患者血小板胞浆游离钙（[Ca2+]i）高于血压正常者（分别为189±38 nM和138±14 nM；P<0.01）。原发性高血压患者治疗后的[Ca2+]i降至138±19 nM。依那普利治疗后血浆肾素活性显著升高。虽然血浆离子钙浓度未改变，但依那普利治疗后甲状旁腺激素显著升高（从0.36±0.22至0.58±0.32 ng/ml，P<0.05）。在安慰剂期，最小血管阻力与[Ca2+]i相关（r=0.62，P<0.01）。最小血管阻力变化与[Ca2+]i变化之间存在密切关系（r=0.78，P<0.01）；然而，最小血管阻力变化与血压、儿茶酚胺或甲状旁腺激素变化无关。（摘要截短至250字）
