To study the acute effects of locally applied static magnetic fields on pharmacologically altered blood pressure in a central artery of the ear lobe of a conscious rabbit.
Hypotensive and vasodilator actions were induced by a calcium channel blocker, nicardipine. Hypertensive and vasoconstrictive actions were induced by a nitric oxide synthase (NOS) inhibitor, L-NAME (NG-nitroarginine methyl ester).
Six experimental procedures were chosen: 1) sham exposure without pharmacological treatment, 2) magnetic field exposure alone, 3) decreased blood pressure induced by injection of nicardipine without magnetic field exposure, 4) decreased blood pressure induced by injection of nicardipine with magnetic field exposure, 5) increased blood pressure induced by L-NAME without magnetic field exposure, and 6) increased blood pressure induced by infusion of L-NAME with magnetic field exposure. .
| Exposure | Parameters |
|---|---|
|
Exposure 1:
Exposure duration:
30 min
|
|
| Frequency | |
|---|---|
| Type | |
| Exposure duration | 30 min |
| Exposure source |
|
|---|---|
| Setup | pair of electromagnets; each consisting of a c-shaped steel bar with 5 coils; ear lobe of the rabbit fixed in the gap of the magnets; upper part of the head and the ear lobes were exposed |
| Sham exposure | A sham exposure was conducted. |
| Measurand | Value | Type | Method | Mass | Remarks |
|---|---|---|---|---|---|
| magnetic flux density | 1 mT | - | - | - | - |
The data revealed that static magnetic fields significantly reduced the vasodilatation with enhanced vasomotion and antagonized the reduction of blood pressure via nicardipine-blocked calcium channels in vascular smooth muscle cells. Additionally, static magnetic fields significantly attenuated the vasoconstriction and suppressed the elevation of blood pressure via nitric oxide synthase (NOS) inhibition in vascular endothelial cells and/or central nervous system neurons.
These data indicate that these modulatory effects of static magnetic fields on blood pressure might involve a feedback control system for alteration in nitric oxide synthase (NOS) activity in conjunction with modulation of calcium dynamics.
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