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SPIN‐LABELLING STUDY OF BIOMEMBRANES IN SPONTANEOUSLY HYPERTENSIVE RATS: CALCIUM‐ AND CALMODULIN‐DEPENDENT REGULATION
Author(s) -
Tsuda Kazushi,
Minatogawa Yohsuke,
Iwahashi Hideo,
Nishio Ichiro,
Kido Ryo,
Masuyama Yoshiaki
Publication year - 1995
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1995.tb02897.x
Subject(s) - electron paramagnetic resonance , chemistry , calmodulin , endocrinology , medicine , verapamil , calcium , spin label , ionophore , hyperfine structure , membrane fluidity , diltiazem , membrane , antagonist , biophysics , nuclear magnetic resonance , biochemistry , receptor , biology , physics , quantum mechanics
Summary 1. The present study was performed to investigate alterations in membrane characteristics of spontaneously hypertensive rats (SHR) by using an electron paramagnetic resonance (EPR) and spin‐labelling methods. 2. Washed erythrocytes from SHR were examined and compared with erythrocytes from age‐matched normotensive Wistar‐Kyoto (WKY) rats. 3. The values of outer hyperfine splitting (2T' ll ) and that of the order parameter (S) obtained from EPR spectra for a spin label agent (5‐nitroxide stearate) were significantly higher in the erythrocytes of SHR than in those of WKY rats. 4. When calcium (Ca 2+ ) was loaded to erythrocytes with a Ca 2+ ionophore (A 23187), the order parameter (S) of the EPR spectra showed a greater increase in SHR than in WKY rats. Furthermore, the Ca 2+ ‐induced change in the order parameter (S) of SHR was significantly antagonized by pretreatment of the Ca 2+ antagonists (verapamil, diltiazem) and a calmodulin antagonist (W‐7). 5. The results show that the erythrocyte membranes of SHR tolerated different spin motions from those of normotensive WKY rats in the EPR study, which might be associated with the idea that the membrane fluidity might be lower in SHR. Furthermore, the data suggest that Ca 2+ ‐calmodulin antagonists may ameliorate the Ca 2+ ‐induced changes in membrane functions in hypertension.