Membrane microviscosity, blood pressure and cytosolic pH in Dahl rats: the influence of plasma lipids.
OBJECTIVE
To determine the relationships between blood pressure, membrane microviscosity, plasma lipids and cytosolic pH in Dahl rats susceptible or resistant to salt hypertension.


METHODS
Blood pressure, plasma triglycerides and total cholesterol, platelet cytosolic pH (pHi) and the microviscosity of both outer membrane leaflet (TMA-DPH fluorescence anisotropy) and membrane lipid core (DPH fluorescence anisotropy) were studied in platelets and erythrocyte ghosts of Dahl salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) rats fed either a low-salt diet (0.3% NaCl) until the age of 9, 15 or 24 weeks or a high-salt diet (4% NaCl) for 5 or 10 weeks after weaning.


RESULTS
At low salt intake, DPH but not TMA-DPH anisotropy increased with age in platelets of SS/Jr rats. Chronic high salt intake was accompanied by an increase of DPH anisotropy in platelets but not in erythrocyte ghosts of SS/Jr rats. Platelet DPH anisotropy correlated positively with blood pressure of salt-loaded SS/Jr rats. Chronic high salt intake also reduced pHi in platelets, the regulation of which seemed to be related to the changes in TMA-DPH anisotropy. This especially concerns the thrombin-induced pHi rise which was inversely related to basal pHi, plasma lipids and TMA-DPH anisotropy. Altered membrane lipid composition might be the underlying mechanism because both membrane microviscosity and platelet pHi regulation were reported to correlate significantly with plasma triglycerides and/or cholesterol.


CONCLUSIONS
Platelets of salt hypertensive Dahl rats are characterized by an increased microviscosity of membrane lipid core which correlated positively with blood pressure. The major influence of plasma triglycerides on DPH anisotropy should be taken into consideration when investigating the links between membrane microviscosity and blood pressure. On the other hand, the changes in microviscosity of the outer membrane leaflet might be involved in pHi regulation (probably through control of the Na+/H+ exchanger).
Zicha
J
J
Institute of Physiology, Academy of Sciences of the Czech Republic, Prague. zicha@biomed.cas.cz
Sang
K H
KH
Kunes
J
J
Devynck
M A
MA
D000821:Animal Feed; D000818:Animals; D001792:Blood Platelets / Q000378:metabolism*; D001794:Blood Pressure; D001809:Blood Viscosity; D003600:Cytosol / Q000378:metabolism; D004161:Diphenylhexatriene / Q000031:analogs & derivatives; D004910:Erythrocyte Membrane / Q000378:metabolism*; D005456:Fluorescent Dyes; D005500:Follow-Up Studies; D006863:Hydrogen-Ion Concentration; D006973:Hypertension / Q000097:blood* / Q000175:diagnosis; D008055:Lipids / Q000097:blood*; D008297:Male; D051381:Rats; D020303:Rats, Inbred Dahl; D017673:Sodium Chloride, Dietary / Q000008:administration & dosage; D017923:Sodium-Hydrogen Exchangers / Q000097:blood
D005456:Fluorescent Dyes; D008055:Lipids; D017673:Sodium Chloride, Dietary; D017923:Sodium-Hydrogen Exchangers; D004161:Diphenylhexatriene; C033628:1-(4-(trimethylamino)phenyl)-6-phenylhexa-1,3,5-triene