Attenuated vasodilator responses to Mg2+ in young patients with borderline hypertension.
Attenuated vasodilator responses to Mg2+ in young patients with borderline hypertension.
复制标题
患有边缘性高血压的年轻患者对 Mg2 的血管舒张反应减弱。
作者：
T. Fujita;Y. Ito;K. Ando;Hiroshi Noda;E. Ogata
应用静脉闭塞体积描记术测定19例青年交界性高血压(BHT)患者和22例年龄匹配的正常血压者(NT)前臂动脉内注入硫酸镁和氯化钾的血流反应，研究其对镁、钾离子的反应。BHT患者输注镁离子后前臂血管阻力下降的百分率显著低于正常对照组(分别为-37.2+/-4.2%和-53.0+/-2.0%，p<0.05；在0.2MEQ/min镁离子输注时，-52.2+/-4.3%和-65.6+/-1.5%，p<0.05)。此外，在10名BHT受试者中，有6名受试者的镁离子反应幅度与初始血管阻力的关系高于11名NT受试者反应点预测值的95%可信区间，这表明在相当大比例的BHT受试者中，镁离子的血管扩张反应减弱。相比之下，9名BHT受试者中有8名对K+的反应点落在95%的可信区间内，这表明大多数BHT受试者对K+的血管扩张反应正常。此外，在正常志愿者中，研究了局部血钙浓度的小幅增加对镁(+)和钾(+)诱导的血管扩张的影响。等量CaCl2溶液以0.09meq/min的速度注入同一臂动脉时，镁离子的扩张作用明显减弱(-30.1meq/-6.5%比-65.8+/-3.2%，p<0.01)，但不影响K+的扩张作用(-63.1meq/min比-55.9meq/min比-55.9+/-3.8%)。提示镁离子的血管扩张作用可能是由于镁离子对钙离子的拮抗作用，而钾离子的血管扩张作用可能与钙离子的运动没有直接关系。因此，BHT受试者对镁离子的这些反应减弱，而对K+的反应正常，可能表明血管镁代谢存在潜在的缺陷，最终可能与质膜处理钙的变化有关，而不是与膜Na(+)-K+泵活性的异常有关。
Limb vascular responses to magnesium (Mg2+) and potassium (K+) ions were studied in 19 young patients with borderline hypertension (BHT) and compared with those of 22 age-matched normotensive subjects (NT) by measuring the forearm blood flow response to intra-arterial infusion of magnesium sulfate and potassium chloride using venous occlusion plethysmography. Percent decrements of forearm vascular resistance with Mg2+ infusions were significantly less in BHT subjects than in NT (-37.2 +/- 4.2% versus -53.0 +/- 2.0%, p less than 0.05, during the infusion of 0.1 meq Mg2+/min, and -52.2 +/- 4.3% versus -65.6 +/- 1.5%, p less than 0.05, during the infusion of 0.2 meq Mg2+/min). Moreover, the relation of the magnitude of Mg2+ response to initial vascular resistance in six of 10 BHT subjects lies above the 95% confidence interval for predicted values calculated for response points in 11 NT subjects, suggesting attenuated vasodilator responses of Mg2+ in a significant proportion of BHT subjects. In contrast, the response points to K+ in eight of nine BHT subjects fall within the 95% confidence interval, suggesting normal vasodilator responses to K+ in the majority of BHT subjects. Furthermore, the effect of small increments in local serum calcium concentrations on Mg2(+)- and K(+)-induced vasodilation was studied in normal volunteers. Isosmolar CaCl2 solution infused into the same brachial artery at a rate of 0.09 meq/min severely blunted the vasodilating actions of Mg2+ (-30.1 +/- 6.5% versus -65.8 +/- 3.2%, p less than 0.01, during the infusion of 0.2 meq Mg2+/min) but did not affect those of K+ (-63.1 +/- 3.1% versus -55.9 +/- 3.8%, NS, during the infusion of 0.154 meq K+/min). It appears that Mg2(+)-induced vasodilation should be due to the antagonistic action of Mg2+ to calcium, but K(+)-induced vasodilation might not be directly related to calcium movement. Thus, these attenuated responses to Mg2+ but normal responses to K+ in BHT subjects may indicate an underlying defect in vascular Mg2+ metabolism, which ultimately may be related to the alterations in calcium handling by plasma membranes rather than to the abnormalities of membrane Na(+)-K+ pump activity.
DOI：
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发表时间：
1981
期刊：
Federation proceedings
影响因子：
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作者：
Potter,JD;Robertson,SP;Johnson,JD
通讯作者：
Johnson,JD