Effect of fusaric acid on phosphoinositide metabolism of erythrocyte membranes of spontaneously hypertensive rats

1986 ◽  
Vol 102 (5) ◽  
pp. 1543-1544
Author(s):  
G. V. Kiselev ◽  
A. N. Minenko ◽  
P. Oehme
1984 ◽  
Vol 66 (6) ◽  
pp. 717-723 ◽  
Author(s):  
I. Aracon-Birlouez ◽  
T. Montenay-Carestier ◽  
M. A. Devynck

1. Fluorescence Dolarization of dbhenvlhexa-triene embedded in membranes was used as an index of ‘microviscosity’ in platelets and ervthro—cyte ghosts of spontaneously hypertensive rats of the Okamoto-Aoki strain (SHR), Wistar-Kyoto strain (WKY) and of the hypertension-prone and -resistant Sabra strains (SBH and SBN), and the original Sabra strain (SB). 2. Microviscosity was increased both in erythrocyte ghosts and platelet membranes of male but not female SHR rats compared with WKY rats and in hypertension-prone Sabra rats compared with the original Sabra rats. 3. Acute and chronic salt loading increased the microviscosity of platelet membranes in all strains of rats but had no effect on the erythrocyte membranes. 4. Microviscosities of vesicles made of lipids extracted from SHR and WKY erythrocyte ghosts were similar. This supports the hypothesis that membrane proteins play a major role in the differences in microviscosity observed in SHR rats.


2001 ◽  
Vol 79 (9) ◽  
pp. 779-784 ◽  
Author(s):  
Ibert C Wells ◽  
Alan J Blotcky

Some essential hypertensive patients and genetic hypertensive rat strains have less than the normal levels of Mg2+ tightly bound to the plasma membranes of their erythrocytes and other cells, i.e., the magnesium binding defect (MgBD). This binding defect appears to cause increased passive permeability of the membrane to Na+ and thereby its increased intracellular concentration, particularly if the Na+-extrusion enzyme systems of the cell are also defective. The Na+-Ca2+ exchange system in the cell membrane exports Na+ and imports Ca2+, increasing the tone of the smooth muscle cell and thus producing hypertension (HTn). This HTn is Na+-sensitive. Evidence supporting this postulate was obtained by determining the intraerythrocyte total concentrations of Na+, Ca2+, K+, and Mg2+ in two strains of spontaneously hypertensive rats (SHR and SS/Jr rats, having the MgBD together with the other requisites of the Na+-sensitive pathway) and their respective controls (WKY and SR/Jr rats, in which this complete pathway is absent). The Na+ and Ca2+ concentrations in the hypertensive rats were increased, and that of K+ was decreased. The concentrations of these cations were very similar in the two hypertensive strains. The level of membrane tightly bound Ca2+ in SHR erythrocyte membranes was significantly higher than those in the other three rat strains, which were not statistically different from each other. These results support previously reported evidence of the existence of a novel HTn-generating mechanism in the SHR rat, in which the intracellular Ca2+ concentration is increased as the result of the enhanced diffusion of this ion into the cell and the accompanying deficiency of the Ca2+ extrusion enzyme systems. This pathway is therefore Na+-insensitive, i.e., Ca2+-sensitive.Key words: essential hypertension, Na+-sensitive hypertension, Na+-insensitive hypertension, Ca2+-sensitive hypertension.


1978 ◽  
Vol 19 (4) ◽  
pp. 597-598 ◽  
Author(s):  
Yukio YAMORI ◽  
Yasuo NARA ◽  
Ryoichi HORIE ◽  
Michiya OHTAKA ◽  
Kiyoe OHTA ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document