To examine the hypothesis that a moderate intensity static magnetic field may influence Ca2+ dynamics in nicardipine (a voltage-gated Ca2+ ion channel blocker)-induced hypotensive SHR (spontaneously hypertensive rat) and modulate reduced blood pressure. This investigation was designed to evaluate the effects of local application of the moderate intensity static magnetic field on pharmacologically modulated blood pressure in the development of genetic hypertension and to elucidate how the static magnetic field influences cardiovascular parameters and Ca2+-related biological pathways and responses.
Four experimental groups of 14 animals each were examined: (1) sham exposure with saline injection (control); (2) static magnetic field exposure with saline injection; (3) sham exposure with nicardipine injection; (4) static magnetic field exposure with nicardipine injection.
Nicardipine (2 mg/kg) was administered three times a week for 14 weeks, and then 15 min after each injection measurements were performed.
Four experimental groups of 14 animals each were examined: (1) sham exposure with intraperitoneal (ip) saline injection control);(2) SMF exposure with ip saline injection (SMF); (3) sham exposure with ip nicardipine injection (NIC); (4) SMF exposure with ip nicardipine injection.
|Setup||The magnet was surgically implanted in the vicinity adjacent to the left carotid sinus baroreceptor region in the neck. As sham exposed controls, a dummy magnet of the same size, weight, and material as the real magnet was implanted in the same position of each rat . The surfaces of both real and dummy magnets were coated with PTFE (Teflon) to use biomedical implant.|
|Additional info||The north side of the magnet was oriented towards the left carotid artery and the nearest distances from the edge of the magnet to the left carotid sinus were 2-3 mm. The principal axis of the left carotid artery was directed perpendicular to the SMF.|
The action of nicardipine significantly decreased blood pressure, and increased heart rate, skin blood flow, skin blood velocity, plasma epinephrine and norepinephrine in the nicardipine group compared with the control group without changing plasma nitric oxide metabolite levels.
Local application of a moderate intensity static magnetic field for 5-8 weeks suppressed or delayed the blood pressure elevation in SHR. The static magnetic field acted synergistically with nicardipine-induced hypotension during 1-8 week exposure periods. Moreover, the static magnetic field induced a significant increase in plasma nitric oxide in the nicardipine-induced hypotension.
These findings indicate that the static magnetic field may enhance nicardipine-induced hypertension by more effectively antagonizing the Ca2+ influx through the Ca2+ channels compared with the nicardipine treatment alone. Furthermore, the enhanced antihypertensive effects of the static magnetic field on the nicardipine-treated rats may be partially related to increased nitric oxide metabolite levels.
Theoretical considerations suggest that the applied static magnetic field can be converted into a changing magnetic field in the baroreceptor region by means of the carotid artery pulsation. The authors propose that the moderate intensity changing magnetic field modulated by the changing pulse rate may influence the activity of baroreceptor and baroreflex function.