<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Berenyiova A</submitter><funding>Scientific Grant Agency of the Ministry of Education, Science, Research and Sport of the Slovak Republic</funding><funding>Slovak Research and Development Agency</funding><pagination>38</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8773407</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>10(1)</volume><pubmed_abstract>Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infects host cells through angiotensin-converting enzyme 2 (ACE2). Concurrently, the product of ACE2 action, angiotensin 1-7 (Ang 1-7), binds to Mas receptors within the cardiovascular system and provides protective effects. Therefore, it is crucial to reveal the role of ACE2 inhibition, especially within pre-existing cardiovascular pathologies. In our study, we imitated the action of SARS-CoV-2 in organisms using the low dose of the ACE2 inhibitor MLN-4760 with the aim of investigating to what degree ACE2 inhibition is detrimental to the cardiovascular system of spontaneously hypertensive rats (SHRs), which represent a model of human essential hypertension. Our study revealed the complex action of MLN-4760 in SHRs. On the one ha</pubmed_abstract><journal>Biomedicines</journal><pubmed_title>Vascular Effects of Low-Dose ACE2 Inhibitor MLN-4760-Benefit or Detriment in Essential Hypertension?</pubmed_title><pmcid>PMC8773407</pmcid><funding_grant_id>PP-COVID-20-0043, APVV-20-0421</funding_grant_id><funding_grant_id>VEGA 2/0111/19</funding_grant_id><pubmed_authors>Balis P</pubmed_authors><pubmed_authors>Cacanyiova S</pubmed_authors><pubmed_authors>Zemancikova A</pubmed_authors><pubmed_authors>Golas S</pubmed_authors><pubmed_authors>Krskova K</pubmed_authors><pubmed_authors>Valaskova Z</pubmed_authors><pubmed_authors>Cebova M</pubmed_authors><pubmed_authors>Dayar E</pubmed_authors><pubmed_authors>Drobna M</pubmed_authors><pubmed_authors>Liskova S</pubmed_authors><pubmed_authors>Berenyiova A</pubmed_authors><pubmed_authors>Bernatova I</pubmed_authors><pubmed_authors>Zorad S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Vascular Effects of Low-Dose ACE2 Inhibitor MLN-4760-Benefit or Detriment in Essential Hypertension?</name><description>Severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infects host cells through angiotensin-converting enzyme 2 (ACE2). Concurrently, the product of ACE2 action, angiotensin 1-7 (Ang 1-7), binds to Mas receptors within the cardiovascular system and provides protective effects. Therefore, it is crucial to reveal the role of ACE2 inhibition, especially within pre-existing cardiovascular pathologies. In our study, we imitated the action of SARS-CoV-2 in organisms using the low dose of the ACE2 inhibitor MLN-4760 with the aim of investigating to what degree ACE2 inhibition is detrimental to the cardiovascular system of spontaneously hypertensive rats (SHRs), which represent a model of human essential hypertension. Our study revealed the complex action of MLN-4760 in SHRs. On the one ha</description><dates><release>2021-01-01T00:00:00Z</release><publication>2021 Dec</publication><modification>2025-05-29T21:12:03.928Z</modification><creation>2025-05-29T21:12:03.928Z</creation></dates><accession>S-EPMC8773407</accession><cross_references><pubmed>35052717</pubmed><doi>10.3390/biomedicines10010038</doi></cross_references></HashMap>