Is renal ß-adrenergic-WNK4-NCC pathway important in salt hypertension of Dahl rats?
Jazyk angličtina Země Česko Médium print-electronic
Typ dokumentu časopisecké články
PubMed
31647304
DOI
10.33549/physiolres.934334
PII: 934334
Knihovny.cz E-zdroje
- MeSH
- beta blokátory terapeutické užití MeSH
- hypertenze chemicky indukované farmakoterapie metabolismus MeSH
- krevní tlak účinky léků fyziologie MeSH
- krysa rodu Rattus MeSH
- kuchyňská sůl aplikace a dávkování škodlivé účinky MeSH
- potkani inbrední Dahl MeSH
- propranolol farmakologie terapeutické užití MeSH
- protein-serin-threoninkinasy metabolismus MeSH
- rodina nosičů rozpuštěných látek 12, člen 1 metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- mužské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- Názvy látek
- beta blokátory MeSH
- kuchyňská sůl MeSH
- propranolol MeSH
- protein-serin-threoninkinasy MeSH
- rodina nosičů rozpuštěných látek 12, člen 1 MeSH
- Slc12a1 protein, rat MeSH Prohlížeč
- Wnk4 protein, rat MeSH Prohlížeč
In 2011 Fujita and coworkers proposed that ß-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-Cl cotransporter (NCC) which participates in salt sensitivity and salt hypertension development in rodents. The aim of our study was to investigate whether the above hypothesis is also valid for salt hypertension of Dahl rats, which are characterized by high sympathetic tone and abnormal renal sodium handling. Male 8-week-old salt-sensitive (SS/Jr) and salt-resistant (SR/Jr) Dahl rats were fed either low-salt diet (LS, 0.4 % NaCl) or high-salt diet (HS, 4 % NaCl) for 6 weeks. Half of the animals on either diet were chronically treated with non-selective ß-blocker propranolol (100 mg/kg/day). At the end of the experiment diuresis and sodium excretion were measured prior and after hydrochlorothiazide injection (HCTZ, 10 mg/kg i.p.). Furthermore, blood pressure (BP), heart rate (HR), sympathetic (pentolinium 5 mg/kg i.v.) and NO-dependent (L-NAME 30 mg/kg i.v.) BP components were determined. Chronic HS diet feeding increased BP through sympathoexcitation in SS/Jr but not in SR/Jr rats. Concomitant propranolol treatment did not lower BP in either experimental group. Under the conditions of low salt intake HCTZ increased diuresis, natriuresis and fractional sodium excretion in SR/Jr but not in SS/Jr rats. HS diet feeding attenuated renal response to HCT in SR/Jr rats, whereas no HCTZ effect was observed in SS/Jr rats fed HS diet. Propranolol treatment did not modify diuresis or natriuresis in any experimental group. In conclusions, our present data do not support the idea on the essential importance of renal ß-adrenergic-WNK4-NCC pathway in pathogenesis and/or maintenance of salt hypertension in Dahl rats.
Citace poskytuje Crossref.org
Contribution of sympathetic nervous system to high blood pressure in salt hypertensive dahl rats