The alteration of red cell Na+ content (Na+i), its causes and the possible relationship to the development of DOCA-salt hypertension were studied in Brattleboro rats. A pronounced hypertension developed in heterozygous (non-DI) animals that synthesize vasopressin (VP) although no substantial Na+i elevation was observed in their erythrocytes. In contrast, Na+i rose progressively in red cells of homozygous VP-deficient (DI) rats in which only marginal increase of systolic blood pressure was found after six weeks of DOCA-salt regimen. DOCA-salt treatment of non-DI rats did not cause major alterations in ouabain-resistant (OR) net Na+ uptake or ouabain-sensitive (OS) net Na+ extrusion but moderately increased furosemide-sensitive (FS) Rb+ uptake. The same treatment of DI rats doubled Na+i by an increased OR net Na+ uptake (due to a major elevation in both Na(+)-K+ cotransport and Na+ leak). Consequently, OS net Na+ extrusion was augmented in red cells of these animals. This was accompanied by an about threefold elevated FS Rb+ uptake. It can be concluded that a) the alterations of OR and/or OS Na+ or K+ transport observed in erythrocytes of Brattleboro DI rats are not essential for the development of severe DOCA-salt hypertension, b) red cell ion transport abnormalities revealed in DOCA-salt treated DI rats might be rather ascribed to cell potassium depletion, and c) increased inward Na(+)-K+ cotransport and Na+ leak causes red cell Na+i elevation that stimulates Na(+)-K+ pump activity.

• MeSH
• aktivní transport účinky léků   MeSH
• bumetanid farmakologie   MeSH
• deoxykortikosteron MeSH
• erytrocyty účinky léků   metabolismus   MeSH
• furosemid farmakologie   MeSH
• hematokrit MeSH
• hemoglobiny metabolismus   MeSH
• hypertenze krev   chemicky indukované   patofyziologie   MeSH
• kinetika MeSH
• krevní tlak MeSH
• krysa rodu Rattus MeSH
• nefrektomie MeSH
• ouabain farmakologie   MeSH
• potkani Brattleboro MeSH
• rubidium krev   MeSH
• sodík dietní * MeSH
• sodík krev   MeSH
• techniky in vitro MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• bumetanid MeSH
• deoxykortikosteron MeSH
• furosemid MeSH
• hemoglobiny MeSH
• ouabain MeSH
• rubidium MeSH
• sodík dietní * MeSH
• sodík MeSH

Our previous study revealed major ion transport alterations that resulted in a pronounced elevation of red cell Na+ content in DOCA-salt treated homozygous vasopressin-deficient (DI) Brattleboro rats in which only a moderate increase of systolic blood pressure occurred. In contrast, no changes of red cell Na+ content were observed in heterozygous vasopressin-secreting (non-DI) Brattleboro rats with a severe DOCA-salt hypertension. Using a chronic supplementation of DI rats with an antidiuretic agonist dDAVP (1-desamino-8-D-arginine vasopressin) we did not demonstrate any significant changes of red cell ion transport in dDAVP-treated DI rats with a fully developed DOCA-salt hypertension. The absence of ion transport alterations seems to be mainly due to dDAVP-induced correction of altered K+ metabolism seen in DOCA-salt treated DI animals. It can be concluded that DOCA-salt hypertension can develop even without red cell ion transport alterations which are usually caused by cell K+ depletion.

• MeSH
• deoxykortikosteron MeSH
• desmopresin aplikace a dávkování   MeSH
• draslík metabolismus   MeSH
• erytrocyty metabolismus   MeSH
• iontový transport MeSH
• krevní tlak MeSH
• krysa rodu Rattus MeSH
• osmolární koncentrace MeSH
• potkani Brattleboro MeSH
• renovaskulární hypertenze metabolismus   MeSH
• sodík metabolismus   MeSH
• tělesná hmotnost MeSH
• vasopresiny nedostatek   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• deoxykortikosteron MeSH
• desmopresin MeSH
• draslík MeSH
• sodík MeSH
• vasopresiny MeSH