Key result
Chronic intermittent hypoxia significantly increased systolic arterial pressure in juvenile rats compared to normoxia (131 vs 115 mmHg, P < 0.05), without reducing cardiac baroreflex gain.
Absolute Event Rate: 131% vs 115%
p-value: p=< 0.05
Chronic intermittent hypoxia induces sympathetic-mediated hypertension in juvenile rats that is driven by enhanced respiratory-sympathetic coupling rather than baroreflex dysfunction.
Supports baroreflex-independent sympathetic hypertension from intermittent hypoxia in juvenile rats; leaves open translation to pediatric OSA.
In the present study, we evaluated the mechanisms underpinning the hypertension observed in freely moving juvenile rats submitted to chronic intermittent hypoxia (CIH). Male juvenile Wistar rats (20-21 days old) were submitted to CIH (6% O(2) for 40 s every 9 min, 8 h day(1)) for 10 days while control rats were maintained in normoxia. Prior to CIH, baseline systolic arterial pressure (SAP), measured indirectly, was similar between groups (86 +/- 1 versus 87 +/- 1 mmHg). After exposure to CIH, SAP recorded directly was higher in the CIH (n = 28) than in the control group (n = 29; 131 +/- 3 versus 115 +/- 2 mmHg, P < 0.05). This higher SAP of CIH rats presented an augmented power of oscillatory components at low (10.05 +/- 0.91 versus 5.02 +/- 0.63 mmHg(2), P < 0.05) and high (respiratory-related) frequencies (12.42 +/- 2.46 versus 3.28 +/- 0.61 mmHg(2), P < 0.05) in comparison with control animals. In addition, rats exposed to CIH also exhibited an increased cardiac baroreflex gain (3.11 +/- 0.08 versus 2.1 +/- 0.10 beats min(1) mmHg(1), P < 0.0001), associated with a shift to the right of the operating point, in comparison with control rats. Administration of hexamethonium (ganglionic blocker, i.v.), injected after losartan (angiotensin II type 1 receptor antagonist) and [beta-mercapto-beta,beta-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2), Arg(8)]-vasopressin (vasopressin type 1a receptor antagonist), produced a larger depressor response in the CIH (n = 8) than in the control group (n = 9; 49 +/- 2 versus 39 +/- 2 mmHg, P < 0.05). Fifteen days after the cessation of exposure to CIH, the mean arterial pressure of CIH rats returned to normal levels. The data indicate that the sympathetic-mediated hypertension observed in conscious juvenile rats exposed to CIH is not secondary to a reduction in cardiac baroreflex gain and exhibits a higher respiratory modulation, indicating that an enhanced respiratory-sympathetic coupling seems to be the major factor contributing to hypertension in rats exposed to CIH.
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Zoccal et al. (2009) studied hypertension (n=57). Chronic intermittent hypoxia (CIH) vs. normoxia was evaluated on Systolic arterial pressure (SAP) (p=< 0.05). Chronic intermittent hypoxia significantly increased systolic arterial pressure in juvenile rats compared to normoxia (131 vs 115 mmHg, P < 0.05), without reducing cardiac baroreflex gain.
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