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The treatment with soluble guanylate cyclase stimulator BAY41-8543 prevents malignant hypertension and associated organ damage

Identifikátory výsledku

  • Kód výsledku v IS VaVaI

    <a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00023001%3A_____%2F25%3A00085621" target="_blank" >RIV/00023001:_____/25:00085621 - isvavai.cz</a>

  • Nalezeny alternativní kódy

    RIV/00216208:11130/25:10496998 RIV/61989592:15110/25:73631832 RIV/00098892:_____/25:10159382 RIV/00064203:_____/25:10496998

  • Výsledek na webu

    <a href="https://journals.lww.com/jhypertension/fulltext/2025/06000/the_treatment_with_soluble_guanylate_cyclase.14.aspx" target="_blank" >https://journals.lww.com/jhypertension/fulltext/2025/06000/the_treatment_with_soluble_guanylate_cyclase.14.aspx</a>

  • DOI - Digital Object Identifier

    <a href="http://dx.doi.org/10.1097/HJH.0000000000004009" target="_blank" >10.1097/HJH.0000000000004009</a>

Alternativní jazyky

  • Jazyk výsledku

    angličtina

  • Název v původním jazyce

    The treatment with soluble guanylate cyclase stimulator BAY41-8543 prevents malignant hypertension and associated organ damage

  • Popis výsledku v původním jazyce

    Objective:Despite availability of an array of antihypertensive drugs, malignant hypertension remains a life-threatening condition, and new therapeutic strategies for the treatment of malignant hypertension and malignant hypertension-associated organ damage are needed. The aim of the present study was to assess the effects of nitric oxide (NO)-independent soluble guanylyl cyclase (sGC) stimulator on the course of malignant hypertension. The second aim was to investigate if the treatment with sodium-glucose cotransporter type 2 (SGLT2) inhibitor would augment the expected beneficial actions of the sGC stimulation on the course of malignant hypertension.Methods:As a model of malignant hypertension, Ren-2 transgenic rats (TGR) treated with nonspecific NO synthase inhibitor (N omega-nitro- l-arginine methyl ester, l-NAME) was used. Blood pressure (BP) was monitored by radiotelemetry, and the treatment was started 3 days before administration of l-NAME.Results:The treatment with sGC stimulator BAY 41-8543, alone or combined with SGLT2 inhibitor empagliflozin, abolished malignant hypertension-related mortality in TGR receiving l-NAME. These two treatment regimens also prevented BP increases after l-NAME administration in TGR, and even decreased BP below values observed in control TGR, and prevented cardiac dysfunction and malignant hypertension-related morbidity. The treatment with the SGLT2 inhibitor empagliflozin did not further augment the beneficial actions of sGC stimulator on the course of malignant hypertension-related mortality.Conclusion:The treatment with NO-independent sGC stimulator displayed marked protective actions on the course of malignant hypertension-related mortality and malignant hypertension-related cardiac damage. This suggests that application of sGC stimulator could be a promising therapeutic means for the treatment of malignant hypertension.

  • Název v anglickém jazyce

    The treatment with soluble guanylate cyclase stimulator BAY41-8543 prevents malignant hypertension and associated organ damage

  • Popis výsledku anglicky

    Objective:Despite availability of an array of antihypertensive drugs, malignant hypertension remains a life-threatening condition, and new therapeutic strategies for the treatment of malignant hypertension and malignant hypertension-associated organ damage are needed. The aim of the present study was to assess the effects of nitric oxide (NO)-independent soluble guanylyl cyclase (sGC) stimulator on the course of malignant hypertension. The second aim was to investigate if the treatment with sodium-glucose cotransporter type 2 (SGLT2) inhibitor would augment the expected beneficial actions of the sGC stimulation on the course of malignant hypertension.Methods:As a model of malignant hypertension, Ren-2 transgenic rats (TGR) treated with nonspecific NO synthase inhibitor (N omega-nitro- l-arginine methyl ester, l-NAME) was used. Blood pressure (BP) was monitored by radiotelemetry, and the treatment was started 3 days before administration of l-NAME.Results:The treatment with sGC stimulator BAY 41-8543, alone or combined with SGLT2 inhibitor empagliflozin, abolished malignant hypertension-related mortality in TGR receiving l-NAME. These two treatment regimens also prevented BP increases after l-NAME administration in TGR, and even decreased BP below values observed in control TGR, and prevented cardiac dysfunction and malignant hypertension-related morbidity. The treatment with the SGLT2 inhibitor empagliflozin did not further augment the beneficial actions of sGC stimulator on the course of malignant hypertension-related mortality.Conclusion:The treatment with NO-independent sGC stimulator displayed marked protective actions on the course of malignant hypertension-related mortality and malignant hypertension-related cardiac damage. This suggests that application of sGC stimulator could be a promising therapeutic means for the treatment of malignant hypertension.

Klasifikace

  • Druh

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

  • CEP obor

  • OECD FORD obor

    30201 - Cardiac and Cardiovascular systems

Návaznosti výsledku

  • Projekt

    Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.

  • Návaznosti

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

Ostatní

  • Rok uplatnění

    2025

  • Kód důvěrnosti údajů

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

Údaje specifické pro druh výsledku

  • Název periodika

    Journal of hypertension

  • ISSN

    0263-6352

  • e-ISSN

    1473-5598

  • Svazek periodika

    43

  • Číslo periodika v rámci svazku

    6

  • Stát vydavatele periodika

    GB - Spojené království Velké Británie a Severního Irska

  • Počet stran výsledku

    12

  • Strana od-do

    1030-1041

  • Kód UT WoS článku

    001488654300023

  • EID výsledku v databázi Scopus

    2-s2.0-105003240913