Am. J. Respir. Crit. Care Med.,
Volume 162, Number 4, October 2000, 1474-1479
Sleep-disordered Respiration in Phenotypically
Normotensive, Genetically Hypertensive Rats
DAVID W.
CARLEY,
KATHLEEN
BERECEK,
ALEKSANDAR
VIDENOVIC,
and
MIODRAG
RADULOVACKI
Departments of Medicine, Pharmacology, and Bioengineering, University of Illinois at Chicago, Chicago, Illinois; and Department of
Physiology and Biophysics, University of Alabama at Birmingham, Birmingham, Alabama
Increased prevalence of sleep-related breathing disorders has
been reported in patients with essential hypertension and we have
described disordered breathing in spontaneously hypertensive rats, an animal model of genetic hypertension. The mechanisms coupling hypertension to respiratory dysfunction during sleep remain, however, largely unknown. To determine if sleep-related respiratory disorder reflects cardiovascular derangement or, alternatively, represents an independent phenotype in hypertensive
rats, we polygraphically recorded groups (n = 10) of genetically
hypertensive, genetically normotensive, and phenotypically normotensive rats carrying a genetic background for hypertension.
Apnea index was elevated more than 15-fold during NREM sleep
in both animal groups carrying hypertension-related genes (p < 0.0001 for each) versus normotensive Wistar Kyoto rats. During
REM sleep, a genetic background for hypertension was associated
with an increased apnea index of at least 500% versus normotensive
Wistar Kyoto rats (p < 0.0001 for each comparison). Still, overall
mean respiratory rate, minute ventilation, and sleep architecture
were equivalent among all animal groups. As expected, blood
pressure and heart period were similar in both normotensive
groups but elevated in the hypertensive animals. Persistent sleep-related breathing disorder despite effective cardiovascular normalization in the phenotypically normotensive but genetically hypertensive rats suggests that disordered breathing represents a
genetically determined phenotype in these animals that is not secondary to the cardiovascular derangements. The model system described here may provide a powerful tool for investigation of the
determinants of sleep-related breathing disorder.
