1. Multiple cell membrane alterations have been described in humans an
d animals with various genetic forms of hypertension and/or dyslipidae
mia, The aim of our study was to characterize membrane microviscosity,
using two different fluorescent probes exploring either the outer mem
brane leaflet [trimethylamino-diphenylhexatriene (TMA-DPH)] or the lip
id membrane core [diphenylhexatriene (DPH)], in platelets and erythroc
ytes of genetically hypertensive rats of the Prague hereditary hypertr
iglyceridaemic (HTG) strain, The relationships of membrane microviscos
ity to hypertension, hypertriglyceridaemia and cell calcium handling w
ere also investigated. 2. Membrane microviscosity was similar in HTG a
nd normotensive control Wistar rats when measured in platelets or eryt
hrocyte ghosts incubated in Na+-containing medium. On the contrary, TM
A-DPH fluorescence anisotropy was significantly reduced in HTG platele
ts incubated in Na+-free medium because external Naf removal elicited
a larger rise of TMA-DPH anisotropy in Wistar platelets. 3. Plasma tri
acylglycerols were associated positively with platelet TMA-DPH anisotr
opy and negatively with DPH anisotropy in both strains, The slopes of
these relationships were reduced in HTG compared with Wistar rats, Pla
telet TMA-DPH anisotropy correlated positively and DPH anisotropy nega
tively with the cytosolic calcium concentration in unstimulated platel
ets, the slopes being almost identical in both strains. 4. Pulse press
ure correlated negatively with TMA-DPH anisotropy and positively with
DPH anisotropy found in erythrocyte ghosts. 5. The present results sug
gest that plasma triacylglycerols and cytosolic calcium are capable of
modulating the membrane microviscosity in this new animal model of ge
netic hypertension associated with hypertriglyceridaemia.