Acute myocardial infarction activates magnocellular vasopressin and oxytocin neurones.

Tytuł:: Acute myocardial infarction activates magnocellular vasopressin and oxytocin neurones.
Autorzy:: Roy RK; Department of Physiology, University of Otago, Dunedin, New Zealand.; Centre for Neuroendocrinology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.; HeartOtago, University of Otago, Dunedin, New Zealand.
Augustine RA; Department of Physiology, University of Otago, Dunedin, New Zealand.; Centre for Neuroendocrinology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.; Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Brown CH; Department of Physiology, University of Otago, Dunedin, New Zealand.; Centre for Neuroendocrinology, School of Biomedical Sciences, University of Otago, Dunedin, New Zealand.; Brain Health Research Centre, University of Otago, Dunedin, New Zealand.
Schwenke DO; Department of Physiology, University of Otago, Dunedin, New Zealand.; HeartOtago, University of Otago, Dunedin, New Zealand.
Źródło:: Journal of neuroendocrinology [J Neuroendocrinol] 2019 Dec; Vol. 31 (12), pp. e12808.
Typ publikacji:: Journal Article; Research Support, Non-U.S. Gov't
Język:: English
Imprint Name(s):: Publication: <2010->: Malden, MA : Wiley & Sons
Original Publication: Eynsham, Oxon, UK : Oxford University Press, c1989-
MeSH Terms:: Myocardial Infarction/*physiopathology
Neurons/*physiology
Oxytocin/*physiology
Paraventricular Hypothalamic Nucleus/*physiology
Supraoptic Nucleus/*physiology
Vasopressins/*physiology
Animals ; Brain Stem/physiology ; Coronary Occlusion/physiopathology ; Male ; Proto-Oncogene Proteins c-fos/biosynthesis ; Rats ; Tyrosine 3-Monooxygenase/metabolism
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Contributed Indexing:: Keywords: myocardial infarction; oxytocin; paraventricular nucleus; supraoptic nucleus; vasopressin
Substance Nomenclature:: 0 (Proto-Oncogene Proteins c-fos)
11000-17-2 (Vasopressins)
50-56-6 (Oxytocin)
EC 1.14.16.2 (Tyrosine 3-Monooxygenase)
Entry Date(s):: Date Created: 20191113 Date Completed: 20201207 Latest Revision: 20201214
Update Code:: 20240105
DOI:: 10.1111/jne.12808
PMID:: 31715034
: Czasopismo naukowe

Pełny tekst

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-Dawley rats were anaesthetised and an acute MI was induced by ligation of the left anterior descending coronary artery. After 90 minutes of myocardial ischaemia, brains were collected. Dual-label immunohistochemistry was used to quantify the expression of Fos protein, a marker of neuronal activation, within vasopressin- or oxytocin-labelled 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 minutes post-MI 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.
(© 2019 British Society for Neuroendocrinology.)

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