Lack of Deficiency in Extracellular and Intralymphocyte Free Mg2+ in Genetically Hypertensive Rats

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Title ( eng )
Lack of Deficiency in Extracellular and Intralymphocyte Free Mg2+ in Genetically Hypertensive Rats
Creator
Sasaki Nobuo
Source Title
Hiroshima Journal of Medical Sciences
Volume 48
Issue 1
Start Page 1
End Page 8
Journal Identifire
[PISSN] 0018-2052
[EISSN] 2433-7668
[NCID] AA00664312
Abstract
Recently it has been suggested that Mg deficiency may play a key role in hypertension and several cardiovascular diseases. In order to investigate the status of Mg in genetic hypertension, the cytosolic free Mg2+ concentration ([Mg2+]i) in the lymphocytes and serum concentrations of free Mg2+ and total Mg were measured in spontaneously hypertensive rats/Izumo (SHR/Izm), stroke-prone spontaneously hypertensive rats/Izumo (SHRSP/Izm), and Wistar-Kyoto rats/Izumo (WKY/Izm). In addition, the basal cytosolic free Ca2+ concentration ([Ca2+]i) was assessed in the three strains. Systolic blood pressure was highest in SHRSP/Izm and lowest in WKY/Izm. No significant differences were found in either the serum free Mg2+ concentrations or the serum total Mg concentrations among WKY/Izm, SHR/Izm, and SHRSP/Izm. [Mg2+]i in the lymphocytes was significantly higher in SHR/Izm than in WKY/Izm (254±51 versus 201±36μmol/liter, p<0.05), but the [Mg2+]i in SHRSP/Izm (211±34μmol/liter) was at the same level as in WKY/Izm. No significant correlation was found between [Mg2+]i in the lymphocytes and systolic blood pressure. Basal [Ca2+]i did not differ among the three strains. Thus, an increase in [Ca2+]i is not obligatory in all cells of genetically hypertensive rats. Mg deficiency may not exist in the intracellular or extracellular space in genetically hypertensive rats.
Keywords
Cytosolic magnesium
Lymphocyte
Mag-fura-2
NDC
Medical sciences [ 490 ]
Language
eng
Resource Type departmental bulletin paper
Publisher
Hiroshima University Medical Press
Date of Issued 1999-03
Publish Type Version of Record
Access Rights open access
Source Identifier
[ISSN] 0018-2052
[NCID] AA00664312