Effects of neck exposure to 5.5 mT static magnetic field on pharmacologically modulated blood pressure in conscious rabbits.
Static magnetic fields (SMF) in the millitesla (mT) range have been reported to modulate microcirculatory hemodynamics and/or blood pressure (BP) under pharmacologically modified state in mammals. This study was designed to investigate the acute effects of local application of a SMF to neck or pelvic region under pharmacologically modulated BP; norepinephrine (NE)-induced hypertension as well as an L-type voltage-gated Ca(2+) channel blocker, nicardipine (NIC)-induced hypotension in conscious rabbits. Magnetic flux densities were up to 5.5 mT and the spatial magnetic gradient peaked in neck (carotid sinus baroreceptor) region at the level of approximately 0.06 mT/mm. The duration of exposure was 30 min (including 10 min of pretreatment) and the effects on BP were investigated up to 100 min postexposure. Baroreflex sensitivity (BRS) was estimated from invasive recordings of systolic BP and pulse interval. Neck exposure to 5.5 mT significantly attenuated the pharmacologically induced vasoconstriction or vasodilation, and subsequently suppressed the increase or decrease in BP compared with sham exposure. In contrast, pelvic exposure to 5.5 mT did not significantly antagonized NE-elevated BP or NIC-reduced BP. The neck exposure to 5.5 mT has a biphasic and restorative effect on vascular tone and BP acting to normalize the tone and BP. The neck exposure to 5.5 mT caused a significant increase in BRS in NE-elevated BP compared with sham exposure. The buffering effects of the SMF on increased hemodynamic variability under NE-induced high vascular tone and NIC-induced low vascular tone might be, in part, dependent on baroreflex pathways, which could modulate NE-mediated response in conjunction with Ca(2+) dynamics.
Okano
Hideyuki
H
Department of Environmental Health, National Institute of Public Health, Saitama, Japan. okano@iic.kyoto-u.ac.jp
Ohkubo
Chiyoji
C
D000818:Animals; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology*; D001919:Bradycardia / Q000139:chemically induced / Q000503:physiopathology; D002121:Calcium Channel Blockers / Q000009:adverse effects; D002346:Carotid Sinus / Q000187:drug effects / Q000502:physiology; D003243:Consciousness; D045462:Endothelium-Dependent Relaxing Factors / Q000097:blood; D006339:Heart Rate / Q000187:drug effects / Q000502:physiology; D006973:Hypertension / Q000139:chemically induced / Q000503:physiopathology*; D007022:Hypotension / Q000139:chemically induced / Q000503:physiopathology*; D008280:Magnetics; D008297:Male; D009333:Neck; D009529:Nicardipine / Q000009:adverse effects; D009569:Nitric Oxide / Q000097:blood; D009638:Norepinephrine / Q000009:adverse effects; D011817:Rabbits; D013610:Tachycardia / Q000139:chemically induced / Q000503:physiopathology; D013997:Time Factors; D014662:Vasoconstrictor Agents / Q000009:adverse effects; D014665:Vasodilator Agents / Q000009:adverse effects; D014666:Vasomotor System / Q000187:drug effects / Q000502:physiology*
D002121:Calcium Channel Blockers; D045462:Endothelium-Dependent Relaxing Factors; D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009569:Nitric Oxide; D009529:Nicardipine; D009638:Norepinephrine