{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,2]],"date-time":"2026-05-02T12:06:17Z","timestamp":1777723577499,"version":"3.51.4"},"reference-count":46,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2019,12,9]],"date-time":"2019-12-09T00:00:00Z","timestamp":1575849600000},"content-version":"vor","delay-in-days":8,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100008247","name":"University of Otago","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100008247","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["J Neuroendocrinology"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Myocardial infarction (MI) is a leading cause of death worldwide. For those who survive the acute insult, the progressive dilation of the ventricle associated with chronic heart failure is driven by an adverse increase in circulating levels of the antidiuretic hormone, vasopressin, which is secreted from hypothalamic supraoptic (SON) and paraventricular nuclei (PVN) nerve terminals. Although increased vasopressin neuronal activity has been demonstrated in the latter stages of chronic heart failure, we hypothesised that vasopressin neurones become activated immediately following an acute MI. Male Sprague\u2010Dawley rats were anaesthetised and an acute MI was induced by ligation of the left anterior descending coronary artery. After 90\u00a0minutes of myocardial ischaemia, brains were collected. Dual\u2010label immunohistochemistry was used to quantify the expression of Fos protein, a marker of neuronal activation, within vasopressin\u2010 or oxytocin\u2010labelled neurones of the hypothalamic PVN and SON. Fos protein and tyrosine hydroxylase within the brainstem were also quantified. The results obtained show that the expression of Fos in both vasopressin and oxytocin neurones of the PVN and SON was significantly elevated as soon as 90\u00a0minutes post\u2010MI compared to sham rats. Moreover, Fos protein was also elevated in tyrosine hydroxylase neurones in the nucleus tractus solitarius and rostral ventrolateral medulla of MI rats than sham rats. We conclude that magnocellular vasopressin and oxytocin neuronal activation occurs immediately following acute MI, rather than in the later stages of chronic heart failure. Therefore, prompt vasopressin antagonist therapy as an adjunct treatment for acute MI may impede the progression of ventricular dilatation, which remains a key adverse hallmark of chronic heart failure.<\/jats:p>","DOI":"10.1111\/jne.12808","type":"journal-article","created":{"date-parts":[[2019,11,12]],"date-time":"2019-11-12T17:15:13Z","timestamp":1573578913000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Acute myocardial infarction activates magnocellular vasopressin and oxytocin neurones"],"prefix":"10.1111","volume":"31","author":[{"given":"Ranjan K.","family":"Roy","sequence":"first","affiliation":[{"name":"Department of Physiology University of Otago Dunedin New Zealand"},{"name":"Centre for Neuroendocrinology School of Biomedical Sciences University of Otago Dunedin New Zealand"},{"name":"HeartOtago University of Otago Dunedin New 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