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Exposure to chronic intermittent hypoxia in rats leads to exaggerated sympatho‐excitatory responses that are buffered by reduced adrenergic vasoconstriction in the mesentery
Author(s) -
Silva Ana Quenia,
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.1051.7
Subject(s) - vasoconstriction , endocrinology , medicine , splanchnic , phenylephrine , propranolol , adrenergic , stimulation , hypoxia (environmental) , chloralose , anesthesia , chemistry , blood pressure , blood flow , receptor , organic chemistry , oxygen
Chronic intermittent hypoxia (CIH) enhances sympatho‐excitatory reflexes in rats with blunted rises in arterial pressure (AP). Phenylephrine (PE; iv) evokes smaller rises in AP, suggesting adrenergic vascular reactivity is reduced. We examined if CIH reduces sympathetically‐mediated vasoconstriction in mesenteric (MES) vascular bed. Male Sprague‐Dawley rats were exposed to CIH (6% O2 for 40s, every 9 min, 8h/day, 2 wks). Under isoflurane rats were ventilated, paralyzed, prepared to record AP, splanchnic SNA, MES artery blood flow and then anesthesia was changed to urethane (750mg/kg)/chloralose (60mg/kg, iv). Compared to controls (n=9), rats with CIH (n=11) had higher AP (127±3 vs 107±7 mmHg, P<0.05) and SNA (85±11 vs 47±5 mV, P<0.05). After CIH, stimulation of brachial nerve evoked larger rises in SNA (137±21 vs 52± 11%, P<0.01) with blunted rises in AP and MES resistance (RES; 110±1 vs 117± 2%, P<0.05). Stimulation of brachial nerve after propranolol induced similar responses, suggesting beta adrenergic receptors were not mediating the blunted effects on AP and MES RES. After ganglionic block to eliminate SNA, PE evoked smaller rises in AP (n=5; 55±9 vs 83±7 mmHg, P<0.05) and MES RES (566±14 vs 971±234 %, P<0.05) in CIH rats. These data suggest CIH reduces sympathetically‐mediated alpha adrenergic vasoconstriction in the mesentery, perhaps as a buffer for chronically elevated SNA. AHA0755292, NIH‐ HL075174