Abstract
The involvement of plasma nitric oxide metabolites (NOx) in hypertension was examined in stroke-resistant spontaneously hypertensive rats during the development of hypertension. Continuous application of a static magnetic field (SMF; a maximum magnetic flux density of 180 millitesla, a peak magnetic gradient of 133 millitesla/mm) to the left carotid sinus baroreceptors of rats was carried out for 6 weeks using a disc-shaped magnetic implant (4.4 mm in diameter, 2.2 mm in height). An L-type voltage-gated Ca2+ channel blocker, nicardipine (2 mg/kg) was administered intraperitoneally three times a week for 6 weeks, and then 15 min after each injection, mean arterial blood pressure (MAP), heart rate (HR), skin blood flow (SBF), skin blood velocity (SBV) and plasma NOx were monitored. The nicardipine significantly decreased MAP, and increased HR, SBF and SBV in the nicardipine-treated rats compared with the control rats (p<0.001) without changing plasma NOx levels. The SMF exposure alone significantly suppressed or retarded the development of hypertension in SMF-exposed rats compared with the control rats (p<0.05). The SMF significantly promoted the nicardipine-induced MAP decrease (p<0.001) and induced a significant increase in plasma NOx levels (p<0.01) in SMF-exposed, nicardipine-treated rats compared with the unexposed, nicardipine-treated rats. The SMF did not significantly induce any changes in the SBF and SBV in nicardipine-treated nor untreated rats. These results suggest that the SMF may enhance nicardipine-induced hypotension by more effectively antagonizing the Ca2+ influx through the Ca2+ channels compared with the nicardipine treatment alone. In addition, the enhanced antihypertensive effects of the SMF on the nicardipine-treated rats might be, at least in part, related to the increased NOx, primarily due to the upregulation of inducible nitric oxide synthase.
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