{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Zhang X"],"funding":["NCATS NIH HHS","NIA NIH HHS","NHLBI NIH HHS"],"pagination":["405-412"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC5798248"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["236"],"pubmed_abstract":["<h4>Background</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<sup>2+</sup>]<sub>i</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.<h4>Methods and results</h4>We measured LV contractility changes after Ang-(1-7) (650ng/kg, iv) and compared myocyte functional an"],"journal":["International journal of cardiology"],"pubmed_title":["Cellular basis of angiotensin-(1-7)-induced augmentation of left ventricular functional performance in heart failure."],"pmcid":["PMC5798248"],"funding_grant_id":["R01 AG049770","R01 HL074318","UL1 TR001420","P01 HL051952"],"pubmed_authors":["Kitzman DW","Cheng HJ","Zhou P","Ferrario CM","Li WM","Zhang X","Cheng CP"],"additional_accession":[]},"is_claimable":false,"name":"Cellular basis of angiotensin-(1-7)-induced augmentation of left ventricular functional performance in heart failure.","description":"<h4>Background</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<sup>2+</sup>]<sub>i</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.<h4>Methods and results</h4>We measured LV contractility changes after Ang-(1-7) (650ng/kg, iv) and compared myocyte functional an","dates":{"release":"2017-01-01T00:00:00Z","publication":"2017 Jun","modification":"2025-04-19T13:14:53.108Z","creation":"2019-03-26T23:39:00Z"},"accession":"S-EPMC5798248","cross_references":{"pubmed":["28096047"],"doi":["10.1016/j.ijcard.2017.01.071"]}}