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Parasymapthetic and sympathetic contributions to enhanced cardiac baroreflex gain after exposure to chronic intermittent hypoxia in rats
Author(s) -
Silva Ana Quenia,
Schreihofer Ann M
Publication year - 2011
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.25.1_supplement.645.17
Short term exposure to chronic intermittent hypoxia (CIH) enhances the gain of baroreflex control of heart rate (HR) in juvenile rats. We examined the relative contributions of sympathetic and parasympathetic control of HR after exposure to CIH. Male Sprague‐Dawley (8wks) rats were exposed to CIH (6% O2 for 40s, every 9 min, 8h/day) for 2 wks. Then they were implanted with femoral arterial and venous catheters that were fed through a tether and swivel system. After 24hrs, the rats were injected with a muscarinic cholinergic blocker (atropine, 3mg//kg) or a β‐adrenergic blocker (propranolol, 4mg/kg). The next day the order of the antagonists was reversed. Arterial pressure was raised and lowered by ~50 mmHg over 1 min by infusions of phenylephrine and nitroprusside before and after antagonism of autonomic inputs to the heart. Baseline and intrinsic HR did not differ between the groups. Rats exposed to CIH (n=5) exhibited enhanced baroreflex gain compared to controls (n=7; slope: 2.76±0.11 vs 2.25±0.23 bpm/min/mmHg, P<0.05). Cholinergic or β‐adrenergic blockade each reduced the slopes to comparable levels in control and CIH rats (atropine: 0.72±0.1 vs 0.79±0.1 bpm/min/mmHg, and propranolol: 0.75±0.13 vs 0.67±0.1 bpm/min/mmHg). These data suggest that parasympathetic and sympathetic inputs both contribute to increased baroreflex gain after short term exposure to CIH. AHA10POST4720006, AHA0755292, NIH‐ HL075174