| http://purl.uniprot.org/citations/17614935 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/17614935 | http://www.w3.org/2000/01/rdf-schema#comment | "In acute myocardial ischemia and in chronic heart failure, sympathetic activation with excessive norepinephrine (NE) release from and reduced NE reuptake into sympathetic nerve endings is a prominent cause of arrhythmias and cardiac dysfunction. The Na(+)/H(+) exchanger NHE1 is the predominant isoform in the heart. It contributes to cellular acid-base balance, and electrolyte, and volume homeostasis, and is activated in response to intracellular acidosis and/or activation of guanine nucleotide binding (G) protein-coupled receptors. NHE1 mediates its signaling via protein kinases A (PKA) or C (PKC). In cardiomyocytes, NHE1 is restricted to specialized membrane domains, where it regulates the activity of pH-sensitive proteins and modulates the driving force of the Na(+)/Ca(2+) exchanger. During acute ischemia/reperfusion and in heart failure the activity/amount of NHE1 is increased, leading to intracellular Ca(2+) overload and promoting structural (apoptosis, hypertrophy) and functional (arrhythmias, hypercontraction) myocardial damage. In sympathetic nerve endings, increased NHE1 activity results in the accumulation of axoplasmic Na(+) that diminishes the inward and/or favors the outward transport of NE via the neuronal norepinephrine transporter (NET). The increased NE levels within the nerve-muscle junction facilitate the sustained stimulation of myocardial alpha- and beta-adrenoceptors (ARs), which in turn aggravate the increases in myocardial NHE1 activity and the associated deleterious effects. Furthermore, the responsiveness of the beta-AR declines overtime, which results in further release of NE, initiating a vicious cycle. Accordingly, NHE1 is a potential candidate for targeted intervention to suppress this feedback loop."xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.org/dc/terms/identifier | "doi:10.1111/j.1527-3466.2007.00010.x"xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/author | "Schulz R."xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/author | "Heusch G."xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/author | "Leineweber K."xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/date | "2007"xsd:gYear |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/name | "Cardiovasc Drug Rev"xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/pages | "123-131"xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/title | "Regulation and role of the presynaptic and myocardial Na+/H+ exchanger NHE1: effects on the sympathetic nervous system in heart failure."xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://purl.uniprot.org/core/volume | "25"xsd:string |
| http://purl.uniprot.org/citations/17614935 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/17614935 |
| http://purl.uniprot.org/citations/17614935 | http://xmlns.com/foaf/0.1/primaryTopicOf | https://pubmed.ncbi.nlm.nih.gov/17614935 |
| http://purl.uniprot.org/uniprot/P32418#attribution-841F0760F78152768D6E7237F36FA496 | http://purl.uniprot.org/core/source | http://purl.uniprot.org/citations/17614935 |