Membrane microviscosity, blood pressure and cytosolic pH in Dahl rats: the influence of plasma lipids
Language English Country Netherlands Media print
Document type Comparative Study, Journal Article, Research Support, Non-U.S. Gov't
- MeSH
- Cytosol metabolism MeSH
- Diphenylhexatriene analogs & derivatives MeSH
- Erythrocyte Membrane metabolism MeSH
- Fluorescent Dyes MeSH
- Hypertension blood diagnosis MeSH
- Hydrogen-Ion Concentration MeSH
- Blood Pressure * MeSH
- Animal Feed MeSH
- Rats MeSH
- Sodium Chloride, Dietary administration & dosage MeSH
- Lipids blood MeSH
- Sodium-Hydrogen Exchangers blood MeSH
- Follow-Up Studies MeSH
- Rats, Inbred Dahl MeSH
- Blood Platelets metabolism MeSH
- Blood Viscosity * MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Male MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Comparative Study MeSH
- Names of Substances
- 1-(4-(trimethylamino)phenyl)-6-phenylhexa-1,3,5-triene MeSH Browser
- Diphenylhexatriene MeSH
- Fluorescent Dyes MeSH
- Sodium Chloride, Dietary MeSH
- Lipids MeSH
- Sodium-Hydrogen Exchangers MeSH
OBJECTIVE: To determine the relationships between blood pressure, membrane microviscosity, plasma lipids and cytosolic pH in Dahl rats susceptible or resistant to salt hypertension. DESIGN AND 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).
References provided by Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
