The relative frequencies of NOS-1,-2, and -3, and EDN-1,-2,-3,-EDNRA, and-EDNRB genotypes were evaluated in 608 subjects [128 with OSA, and 480 without OSA (NOSA)].
The result showed that there was a significant reduction in ET-1 levels in OSA patients before and after CPAP therapy (SMD = - 0.74, 95% CI = - 1.30 to - 0.17, z = 2.56, p = 0.01).
HIF-1 and its target gene endothelin-1 (ET-1) are activated by intermittent hypoxia (IH), one of the main consequences of obstructive sleep apnea (OSA), and both play a key role in the cardiovascular consequences of IH.
While it is recognized that the balance between vasoconstrictive (endothelin-1) and vasodilatory molecules (nitric oxide, NO) determine vascular profile, molecular mechanisms contributing to vascular dysfunction and IR in OSA are not completely understood.
Main mechanisms involved in the ocular complications of OSA are related to intermittent hypoxia, sympathetic system activation, oxidant stress, and deleterious effects of endothelin 1.
Furthermore, the carotid IMT of patients with OSAHS was significantly correlated with AHI (P=0.037), plasma ET-1 (P=0.001), plasma NO (P<0.001), BPV LF before retiring (P<0.001).
GAX was a target gene of miR-130a.Compared with the normal control group, the relative expression of miR-130a and the serum levels of ET-1 and VEGF were increased, whereas the mRNA expression of GAX and the serum levels of NO and SOD were decreased in the OSAHS-associated PHT group.
The relative frequencies of NOS-1,-2, and -3, and EDN-1,-2,-3,-EDNRA, and-EDNRB genotypes were evaluated in 608 subjects [128 with OSA, and 480 without OSA (NOSA)].
Traits of obstructive sleep apnea syndrome (OSAS) such as impaired ventilatory control, craniofacial abnormalities, and concomitant cardiovascular diseases are associated with modified endothelin-1 gene (EDN-1) or endothelin-receptor-subtype-a (EDNRA) gene.
We investigated a cohort of 364 consecutive patients (age 57 +/- 10 years) with mild to severe OSA for the EDN1 variant Lys198Asn (G/T) and endothelin plasma levels and compared them with 57 controls.
Our study demonstrated that TNF-α 308 G/A, 5-HTT LPR, and 5-HTT-VNTR polymorphisms were associated with OSAS risk, whereas little association was observed between 5-HTR2A 102C/T, 5-HTR2A A1438G, ACE I/D, or LEPR-Gln 223Arg polymorphism and risk of OSAS in the Chinese population.
ACE polymorphism I/D had no statistically significant association with increased OSA risk, but the II genotype of ACE may be a risk factor for OSA with hypertension in Asians.
The frequencies of II genotype (OR = 1.8, 95 % CI 1.26-2.60, p = 0.001) and I allele (OR = 1.4, 95 % CI 1.13-1.69, p = 0.001) of ACE gene were found to be significantly increased in patients with OSA as compared to patients without OSA.
An interaction analysis including sex, ACE I/D polymorphism (DD and ID versus II), and OSA identified a significant interaction between OSA and the ACE I/D polymorphism: odds ratio (OR) 6.3, 95% confidence interval (CI) 1.8-22.5, P = 0.004 as well as between OSA and sex: OR 3.3, 95% CI 1.1-9.6, P = 0.033.