Membrane microviscosity, blood pressure and cytosolic pH in Dahl rats: the influence of plasma lipids
Jazyk angličtina Země Nizozemsko Médium print
Typ dokumentu srovnávací studie, časopisecké články, práce podpořená grantem
- MeSH
- cytosol metabolismus MeSH
- difenylhexatrien analogy a deriváty MeSH
- erytrocytární membrána metabolismus MeSH
- fluorescenční barviva MeSH
- hypertenze krev diagnóza MeSH
- koncentrace vodíkových iontů MeSH
- krevní tlak * MeSH
- krmivo pro zvířata MeSH
- krysa rodu Rattus MeSH
- kuchyňská sůl aplikace a dávkování MeSH
- lipidy krev MeSH
- Na(+)-H(+) antiport krev MeSH
- následné studie MeSH
- potkani inbrední Dahl MeSH
- trombocyty metabolismus MeSH
- viskozita krve * MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- srovnávací studie MeSH
- Názvy látek
- 1-(4-(trimethylamino)phenyl)-6-phenylhexa-1,3,5-triene MeSH Prohlížeč
- difenylhexatrien MeSH
- fluorescenční barviva MeSH
- kuchyňská sůl MeSH
- lipidy MeSH
- Na(+)-H(+) antiport 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).
Citace poskytuje Crossref.org
Research on Experimental Hypertension in Prague (1966-2009)
