<HashMap><database>biostudies-literature</database><scores/><additional><submitter>Zhang X</submitter><funding>NCATS NIH HHS</funding><funding>NIA NIH HHS</funding><funding>NHLBI NIH HHS</funding><pagination>405-412</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC5798248</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>236</volume><pubmed_abstract>&lt;h4>Background&lt;/h4>Angiotensin-(1-7) [Ang-(1-7)] exhibits cardiovascular effects opposite those of angiotensin II (Ang II), thus providing protection against heart disease. However, how Ang-(1-7) imparts cardioprotection is unclear, and its direct cardiac effects are controversial. Whether heart failure (HF) alters cardiac contractile responses to Ang-(1-7) remains undetermined. We tested the hypothesis that in HF, Ang-(1-7) may produce positive modulation on [Ca&lt;sup>2+&lt;/sup>]&lt;sub>i&lt;/sub> regulation, enhancing left ventricular (LV) and myocyte contraction and relaxation via Ang-(1-7) Mas receptor coupled with nitric oxide (NO)/bradykinin (BK)-mediated mechanism.&lt;h4>Methods and results&lt;/h4>We measured LV contractility changes after Ang-(1-7) (650ng/kg, iv) and compared myocyte functional an</pubmed_abstract><journal>International journal of cardiology</journal><pubmed_title>Cellular basis of angiotensin-(1-7)-induced augmentation of left ventricular functional performance in heart failure.</pubmed_title><pmcid>PMC5798248</pmcid><funding_grant_id>R01 AG049770</funding_grant_id><funding_grant_id>R01 HL074318</funding_grant_id><funding_grant_id>UL1 TR001420</funding_grant_id><funding_grant_id>P01 HL051952</funding_grant_id><pubmed_authors>Kitzman DW</pubmed_authors><pubmed_authors>Cheng HJ</pubmed_authors><pubmed_authors>Zhou P</pubmed_authors><pubmed_authors>Ferrario CM</pubmed_authors><pubmed_authors>Li WM</pubmed_authors><pubmed_authors>Zhang X</pubmed_authors><pubmed_authors>Cheng CP</pubmed_authors></additional><is_claimable>false</is_claimable><name>Cellular basis of angiotensin-(1-7)-induced augmentation of left ventricular functional performance in heart failure.</name><description>&lt;h4>Background&lt;/h4>Angiotensin-(1-7) [Ang-(1-7)] exhibits cardiovascular effects opposite those of angiotensin II (Ang II), thus providing protection against heart disease. However, how Ang-(1-7) imparts cardioprotection is unclear, and its direct cardiac effects are controversial. Whether heart failure (HF) alters cardiac contractile responses to Ang-(1-7) remains undetermined. We tested the hypothesis that in HF, Ang-(1-7) may produce positive modulation on [Ca&lt;sup>2+&lt;/sup>]&lt;sub>i&lt;/sub> regulation, enhancing left ventricular (LV) and myocyte contraction and relaxation via Ang-(1-7) Mas receptor coupled with nitric oxide (NO)/bradykinin (BK)-mediated mechanism.&lt;h4>Methods and results&lt;/h4>We measured LV contractility changes after Ang-(1-7) (650ng/kg, iv) and compared myocyte functional an</description><dates><release>2017-01-01T00:00:00Z</release><publication>2017 Jun</publication><modification>2025-04-19T13:14:53.108Z</modification><creation>2019-03-26T23:39:00Z</creation></dates><accession>S-EPMC5798248</accession><cross_references><pubmed>28096047</pubmed><doi>10.1016/j.ijcard.2017.01.071</doi></cross_references></HashMap>