Okano H, Ohkubo C
Department of Physiological Hygiene, National Institute of Public Health, Tokyo, Japan.
Bioelectromagnetics. 2001 Sep;22(6):408-18. doi: 10.1002/bem.68.
Acute effects of locally applied static magnetic fields (SMF) on pharmacologically altered blood pressure (BP) in a central artery of the ear lobe of a conscious rabbit were evaluated. Hypotensive and vasodilator actions were induced by a Ca(2+) channel blocker, nicardipine (NIC). Hypertensive and vasoconstrictive actions were induced by a nitric oxide synthase (NOS) inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME). The hemodynamic changes in the artery exposed to SMF were measured continuously and analyzed by penetrating microphotoelectric plethysmography (MPPG). Concurrently, BP changes in a central artery contralateral to that of the exposed ear lobe were monitored. SMF intensity was 1 mT and the duration of exposure was 30 min. A total of 180 experimental trials were carried out in 34 healthy adult male rabbits weighing 2.6-3.8 kg. Six experimental procedures were chosen at random: (1) sham exposure without pharmacological treatment; (2) SMF exposure alone; (3) decreased BP induced by a single intravenous (iv) bolus injection of NIC (100 microM/kg) without SMF exposure; (4) decreased BP induced by injection of NIC with SMF exposure; (5) increased BP induced by a constant iv infusion of L-NAME (10 mM/kg/h) without SMF exposure; (6) increased BP induced by infusion of L-NAME with SMF exposure. The results demonstrated that SMF significantly reduced the vasodilatation with enhanced vasomotion and antagonized the reduction of BP via NIC-blocked Ca(2+) channels in vascular smooth muscle cells. In addition, SMF significantly attenuated the vasoconstriction and suppressed the elevation of BP via NOS inhibition in vascular endothelial cells and/or central nervous system neurons. These results suggest that these modulatory effects of SMF on BP might, in part, involve a feedback control system for alteration in NOS activity in conjunction with modulation of Ca(2+) dynamics.
评估了局部施加静磁场（SMF）对清醒家兔耳垂中央动脉经药理学改变的血压（BP）的急性影响。通过钙（Ca²⁺）通道阻滞剂尼卡地平（NIC）诱导降压和血管舒张作用。通过一氧化氮合酶（NOS）抑制剂N（ω）-硝基-L-精氨酸甲酯（L-NAME）诱导升压和血管收缩作用。通过穿透式微光电体积描记法（MPPG）连续测量暴露于SMF的动脉中的血流动力学变化并进行分析。同时，监测与暴露耳垂对侧的中央动脉中的血压变化。SMF强度为1 mT，暴露持续时间为30分钟。对34只体重2.6 - 3.8 kg的健康成年雄性家兔进行了总共180次实验。随机选择六个实验程序：（1）无药理学处理的假暴露；（2）单独的SMF暴露；（3）单次静脉注射（iv）尼卡地平（100 μM/kg）诱导的血压降低，无SMF暴露；（4）注射尼卡地平并暴露于SMF诱导的血压降低；（5）持续静脉输注L-NAME（10 mM/kg/h）诱导的血压升高，无SMF暴露；（6）输注L-NAME并暴露于SMF诱导的血压升高。结果表明，SMF通过增强血管运动显著减少血管舒张，并拮抗通过NIC阻断血管平滑肌细胞中Ca²⁺通道引起的血压降低。此外，SMF通过抑制血管内皮细胞和/或中枢神经系统神经元中的NOS，显著减弱血管收缩并抑制血压升高。这些结果表明，SMF对血压的这些调节作用可能部分涉及与Ca²⁺动力学调节相结合的NOS活性改变的反馈控制系统。
