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Hypertension induced by chronic intermittent hypoxia is accompanied by reduced expression of neuronal nitric oxide synthase (nNOS) and angiotensin type 1 receptors (AT1R) in the hypothalamic PVN
Author(s) -
Carreño Flávia Regina,
Calderon Alfred S,
Ji Lisa,
Mifflin Steven W,
Toney Glenn M,
Cunningham J Thomas
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.1017.31
Subject(s) - endocrinology , medicine , angiotensin ii , nitric oxide synthase , hypoxia (environmental) , receptor , renin–angiotensin system , chemistry , nitric oxide , blood pressure , oxygen , organic chemistry
Chronic intermittent hypoxia (CIH) is an animal model of the hypoxemia associated with sleep apnea that is associated with hypertension related to increased sympathetic outflow and activation of the renin‐angiotensin system. This study tested effects of CIH on nNOS and AT1R abundance in the paraventricular nucleus (PVN) and nucleus of the solitary tract (NTS). Adult male rats were exposed to CIH (between 8am and 4pm alternate 21% and 10% O 2 every 3 min) for 7 days. Previous studies have shown that such exposures to CIH significantly elevate blood pressure. On the 8 th day, rats were anesthetized, their brains were removed, and punch samples containing the PVN and NTS were collected. Punches were used for Western Blot analysis for nNOS, AT1R and β‐actin. CIH had no significant effect on nNOS or AT1R expression in the NTS. However, both nNOS and AT1R expression were reduced in the PVN ofCIH rats compared to controls. A separate RT‐QPCR analysis demonstrated a decrease (~15%) in AT1aR mRNAin the PVN of CIH rats. The results obtained from this study suggest that the down‐regulation of nNOS expression in the PVN may contribute to the central mechanism that produce increased sympathetic outflow and hypertension during CIH. Decreased AT 1 receptor expression in the PVN could be a compensatory response related to increased activation. P01 HL088052