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Decreased plasma levels of nitric oxide metabolites, angiotensin II, and aldosterone in spontaneously hypertensive rats exposed to 5 mT static magnetic field
Author(s) -
Okano Hideyuki,
Masuda Hiroshi,
Ohkubo Chiyoji
Publication year - 2005
Publication title -
bioelectromagnetics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.435
H-Index - 81
eISSN - 1521-186X
pISSN - 0197-8462
DOI - 10.1002/bem.20055
Subject(s) - endocrinology , aldosterone , medicine , nitric oxide , saline , angiotensin ii , chemistry , blood pressure , renin–angiotensin system , hormone , intraperitoneal injection , catecholamine
Previously, we found that whole body exposure to static magnetic fields (SMF) at 10 mT ( B max ) and 25 mT ( B max ) for 2–9 weeks suppressed and delayed blood pressure (BP) elevation in young, stroke resistant, spontaneously hypertensive rats (SHR). In this study, we investigated the interrelated antipressor effects of lower field strengths and nitric oxide (NO) metabolites (NO x = NO 2 − + NO 3 − ) in SHR. Seven‐week‐old male rats were exposed to two different ranges of SMF intensity, 0.3–1.0 mT or 1.5–5.0 mT, for 12 weeks. Three experimental groups of 20 animals each were examined: (1) no exposure with intraperitoneal (ip) saline injection (sham‐exposed control); (2) 1 mT SMF exposure with ip saline injection (1 mT); (3) 5 mT SMF exposure with ip saline injection (5 mT). Arterial BP, heart rate (HR), skin blood flow (SBF), plasma NO metabolites (NO x ), and plasma catecholamine levels were monitored. SMF at 5 mT, but not 1 mT, significantly suppressed and retarded the early stage development of hypertension for several weeks, compared with the age matched, unexposed (sham exposed) control. Exposure to 5 mT resulted in reduced plasma NO x concentrations together with lower levels of angiotensin II and aldosterone in SHR. These results suggest that SMF may suppress and delay BP elevation via the NO pathways and hormonal regulatory systems. Bioelectromagnetics 26:161–172, 2005. © 2005 Wiley‐Liss, Inc.