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Is Renal beta-Adrenergic-WNK4-NCC Pathway Important in Salt Hypertension of Dahl Rats?

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F19%3A00565778" target="_blank" >RIV/67985823:_____/19:00565778 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00023001:_____/19:00078908

  • Výsledek na webu

    <a href="http://www.biomed.cas.cz/physiolres/pdf/2019/68_873.pdf" target="_blank" >http://www.biomed.cas.cz/physiolres/pdf/2019/68_873.pdf</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.33549/physiolres.934334" target="_blank" >10.33549/physiolres.934334</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    Is Renal beta-Adrenergic-WNK4-NCC Pathway Important in Salt Hypertension of Dahl Rats?

  • Popis výsledku v původním jazyce

    In 2011 Fujita and coworkers proposed that beta-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-CI 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 % NaCI) or high-salt diet (HS, 4 % NaCI) for 6 weeks. Half of the animals on either diet were chronically treated with non-selective 8-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 beta-adrenergic-WNK4-NCC pathway in pathogenesis and/or maintenance of salt hypertension in Dahl rats.

  • Název v anglickém jazyce

    Is Renal beta-Adrenergic-WNK4-NCC Pathway Important in Salt Hypertension of Dahl Rats?

  • Popis výsledku anglicky

    In 2011 Fujita and coworkers proposed that beta-adrenergic stimulation causes decreased serine/threonine-protein kinase WNK4 transcription leading to the activation of Na-CI 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 % NaCI) or high-salt diet (HS, 4 % NaCI) for 6 weeks. Half of the animals on either diet were chronically treated with non-selective 8-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 beta-adrenergic-WNK4-NCC pathway in pathogenesis and/or maintenance of salt hypertension in Dahl rats.

Klasifikace

  • Druh

    J<sub>imp</sub> - Článek v periodiku v databázi Web of Science

  • CEP obor

  • OECD FORD obor

    30105 - Physiology (including cytology)

Návaznosti výsledku

  • Projekt

    <a href="/cs/project/NV15-25396A" target="_blank" >NV15-25396A: Centrální a periferní modulace cévního tonu a vylučování sodíku: úloha mozku a ledvin v patofyziologii hypertenze</a><br>

  • Návaznosti

    P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)

Ostatní

  • Rok uplatnění

    2019

  • Kód důvěrnosti údajů

    S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Údaje specifické pro druh výsledku

  • Název periodika

    Physiological Research

  • ISSN

    0862-8408

  • e-ISSN

    1802-9973

  • Svazek periodika

    68

  • Číslo periodika v rámci svazku

    6

  • Stát vydavatele periodika

    CZ - Česká republika

  • Počet stran výsledku

    10

  • Strana od-do

    873-882

  • Kód UT WoS článku

    000505181300001

  • EID výsledku v databázi Scopus

    2-s2.0-85077404400