The association of angiotensin converting enzyme (ACE) polymorphisms with sleep apnea and hypertension.

STUDY OBJECTIVES To identify the role of polymorphisms in the angiotensin-converting enzyme (ACE) gene in modulating susceptibility to hypertension in sleep apnea. DESIGN Observational cross-sectional study. PARTICIPANTS Nine hundred seventy-two participants of the Cleveland Family Study who underwent home sleep studies, blood pressure assessments, and genotyping. RESULTS After controlling for age, sex, race, and obesity, hypertension risk was reduced in participants who possess the ACE deletion (D) polymorphism with an odds ratio = 0.63 (95% confidence interval: 0.41-0.96) comparing those with 2 versus no D alleles. In analyses stratified by apnea severity, the protective effect of the D allele was most evident in those with severe apnea. Among subjects with severe apnea, the odds ratios for hypertension were 0.47 (0.22-1.00) for 1 D allele and 0.57 (0.26-1.24) for 2 D alleles. CONCLUSIONS The ACE deletion allele may protect against hypertension in the setting of obstructive sleep apnea. Further research into the potential role of angiotensin in modulating the hypertensive effect of sleep apnea is needed.

[1]  H. Kume,et al.  Angiotensin converting enzyme in patients with sleep apnoea syndrome: plasma activity and gene polymorphisms , 2001, European Respiratory Journal.

[2]  R. Hui,et al.  Angiotensin-converting enzyme gene insertion/deletion (I/D) polymorphism in hypertensive patients with different degrees of obstructive sleep apnea. , 2000, Hypertension research : official journal of the Japanese Society of Hypertension.

[3]  X. Huang,et al.  Angiotensin I-converting enzyme gene polymorphism in Chinese patients with obstructive sleep apnea syndrome. , 1999, Chinese medical journal.

[4]  A. Allen,et al.  Angiotensin AT1 receptor‐mediated excitation of rat carotid body chemoreceptor afferent activity , 1998, The Journal of physiology.

[5]  S. Redline,et al.  The familial aggregation of obstructive sleep apnea. , 1995, American journal of respiratory and critical care medicine.

[6]  Lie Gao,et al.  Angiotensin II enhances carotid body chemoreflex control of sympathetic outflow in chronic heart failure rabbits. , 2006, Cardiovascular research.

[7]  S. Redline,et al.  Predictors of longitudinal change in sleep-disordered breathing in a nonclinic population. , 2003, Sleep.

[8]  P Corvol,et al.  An insertion/deletion polymorphism in the angiotensin I-converting enzyme gene accounting for half the variance of serum enzyme levels. , 1990, The Journal of clinical investigation.

[9]  F. Soubrier,et al.  PCR detection of the insertion/deletion polymorphism of the human angiotensin converting enzyme gene (DCP1) (dipeptidyl carboxypeptidase 1). , 1992, Nucleic acids research.

[10]  T. Young,et al.  Angiotensin-converting enzyme, sleep-disordered breathing, and hypertension. , 2004, American Journal of Respiratory and Critical Care Medicine.