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Changes in neuropeptide expression in hypothalamic neurons of rats with chronic heart failure
Author(s) -
LlewellynSmith Ida J,
Smith Cameron M
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.1008.10
Subject(s) - medicine , endocrinology , vasopressin , hypothalamus , neuropeptide , ventricle , heart failure , enkephalin , receptor , opioid
Pre‐autonomic and neuroendocrine neurons in the hypothalamic paraventricular nucleus (PVN) are important for regulating blood pressure and fluid balance. In chronic heart failure (CHF), changes occur in the anatomy and physiology of the PVN to compensate for reduced heart function. We investigated the effect of CHF on hypothalamic neurons immunoreactive for corticotropin releasing factor (CRF), vasopressin (VP), enkephalin (ENK), pro‐ENK or nitric oxide synthase (NOS). To induce myocardial infarctions that occupied > 40% of the left ventricle, we ligated left coronary arteries in male rats and perfused them 6‐8 weeks later. Hypothalamic sections from CHF rats and control rats without ligations were stained with immunoperoxidase and immunoreactive neurons were counted. We found more CRF‐ and VP‐immunoreactive neurons in the PVN of CHF than control rats (p<0.05, n=5‐6 rats/group). There was also a trend towards a decreased number of NOS‐immunoreactive neurons in the PVN in CHF rats (p=0.07, n=5/group). ENK neurons were not found in the PVN itself but in the anterior hypothalamic area. The number of ENK‐ (p=0.34, n=4/group) and pro‐ENK‐immunoreactive (p=0.57, n=3/group) neurons did not differ between CHF and control rats. These results suggest that CHF causes widespread changes in the neurochemistry of hypothalamic neurons involved in the regulation of autonomic function. Support: NH&MRC of Australia