| Literature DB >> 19429526 |
Jianhua Huang1, Sara Lusina, Tian Xie, Ensheng Ji, Shuanglin Xiang, Yuzhen Liu, J Woodrow Weiss.
Abstract
Exposure to cyclic intermittent hypoxia (CIH) is associated with elevated arterial pressure and sustained sympathoexcitation, but the causes of the augmented sympathetic activity remain poorly understood. We recorded arterial pressure, heart rate, and renal sympathetic nerve (RSN) activity in conscious rats previously exposed to either CIH or Sham for 3 weeks during acute exposure to hypoxia (15% and 10% O(2)) or hypercapnia (7% CO(2)). Hemodynamic responses to both hypercapnia and hypoxia were similar between CIH-exposed and Sham-exposed rats, although the pattern of response was different for hypoxia (tachycardia with no change in arterial pressure) and hypercapnia (bradycardia and increased arterial pressure). RSN responses as a percent of the baseline were, however, significantly greater in CIH-exposed animals (CIH-exposed: 15% O(2) - 123.4+/-0.06%; 10% O(2) - 136.7+/-0.12%; 7% CO(2) - 138.3+/-0.18%; Sham-exposed: 15% O(2) - 106.6+/-0.03%; 10% O(2) - 107.6+/-0.01%; 7% CO(2) - 103.0+/-0.14% P<0.01 for all conditions). These data indicate that in conscious rats exposure to CIH enhances sympathetic responses to both hypoxia and hypercapnia.Entities:
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Year: 2009 PMID: 19429526 DOI: 10.1016/j.resp.2009.02.010
Source DB: PubMed Journal: Respir Physiol Neurobiol ISSN: 1569-9048 Impact factor: 1.931