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Hypotension‐induced expression of c‐fos in the rostral ventrolateral medulla of lean and obese Zucker rats
Author(s) -
Guimaraes Priscila S,
Schreihofer Ann M
Publication year - 2010
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.24.1_supplement.808.1
Subject(s) - rostral ventrolateral medulla , medicine , endocrinology , tyrosine hydroxylase , chemistry , saline , catecholaminergic cell groups , catecholaminergic , heart rate , immunohistochemistry , blood pressure , catecholamine
In obese Zucker rats (OZR) acute decreases in arterial pressure (AP) evoke blunted rises in sympathetic nerve activity (SNA) and heart rate (HR) compared to lean Zucker rats (LZR). We hypothesized that hypotension‐induced activation of neurons in rostral ventrolateral medulla (RVLM), the source of drive for SNA, would be less in OZR vs. LZR. Conscious rats with arterial and venous catheters received hydralazine (HDZ; 6.8–15 mg/kg/2 ml/60s, iv) to reduce AP or saline. After 90 min rats were transcardially perfused with formaldehyde. Baseline mean AP was higher in OZR (n=12) vs. LZR (n=13: 124 ± 2 vs. 114 ± 2 mmHg, P<0.001). HDZ reduced mean AP comparably in LZR and OZR for the 90‐min period. The initial rise in HR was blunted in OZR, but by 5 min the rise in HR was comparable. Immunohistochemistry of brain stem sections to identify activation (c‐Fos expression) of catecholaminergic (tyrosine hydroxylase, TH) and non‐C1 RVLM neurons showed that saline evoked minimal Fos expression. In contrast, HDZ evoked robust Fos expression in RVLM (OZR= 48.8 ± 2.8; LZR= 52.8 ± 2.2 Fos+ nuclei) with a minority in TH+ neurons (OZR=8.28 ± 0.6; LZR= 10.8 ± 1.0). However, there was no difference between OZR and LZR in counts of c‐Fos+ neurons with or without TH. These results suggest that although OZR may have an attenuated ability to respond to brief changes in AP, their responses to prolonged hypotension are normal. CAPES (1203‐09‐6), NIH ( HL086759 )