Background Hypertension is a common and complex disorder. To identify its susceptibility genes may contribute to genetic screening and treatment for hypertension. Although many large-scale genome-wide association studies have been performed, only a few studies have successfully identified the loci that are related to the hypertension, not to mention the scanty Asian studies. Young-onset hypertension (YOH) may be a more feasible target disorder to investigate than the late-onset one due to its stronger genetic component.Methods We performed a three-stage genome-wide association study to map YOH susceptibility genes. In the first stage, we analyzed 400 YOH cases and 400 age and gender matched controls with BMI adjusted in all the analyses. In the second stage, an independent sample (600 YOH cases and 600 age and gender matched controls) was used to verify the results. Besides the conventional single locus test, Multilocus association tests and pair were used to increase the power to identify potential SNPs. After considering stringent adjustments of multiple testing, 14 SNP septets from the multilocus test and 20 SNP pairs from the epistasis test were selected to verify. In the third stage, gene expression profiles of the genes located in these regions were also tested to further confirm those finding.Results Finally, three genes (GSN, LARS and ACTN4) from the multilocus test and one gene pair (LIPC and CELF5) were verified successfully. Some animal experiments also showed that GSN is involved in the inflammatory processes, which is an important participant in the pathophysiology of hypertension. LIPC plays a major role in the regulation of plasma lipids and is involved in the glycerolipid metabolism. Those genes are novel hypertension targets identified in this YOH GWA study of the Han Chinese population.
L-002 ADENOSINE A 2a RECEPTOR GENE EXPRESSION IN ESSENTIAL HYPERTENSIONBackground Adenosine A 2A receptor (ADORA 2A ) signalling pathway induced vasodilation may have a role in essential hypertension (EH).The study aimed to investigate the expression of ADORA 2A in human blood associated with EH. This could provide new insights into potential development of more selective drugs targeting ADORA 2A .
MethodsThe study utilised samples from 7 hypertensive (HT: male:3, female:4) and 7 normotensive (NT: male:3, female:4) subjects who were unrelated and matched for age AE5 years, gender and ethnicity. Electrocardiography (ECG) was taken in a supine position. Blood samples were collected using the PAXgene blood RNA system. ADORA 2A gene expression levels were detected by real time PCR. 18S rRNA and beta-actin (ACTB) were utilised as housekeeping genes. REST software was employed for data analysis.Results HT subjects were aged 50 AE 2 years old and their blood pressure were 126 AE 4/82 AE 2 mmHg, which were not significantly different to the NT group. Sinus rhythm presented in all participants and none of subjects was suspected having left ventricle hypertrophy (LVH) according to the standard ECG criteria for LVH. Also, t...
The phytochemical screening of the seeds extracts of Picralima nitida has highlighted the presence of alkaloids and terpenes poly sterols in chloroform solutions, methanol and in the aqueous. Unlike chloroform and methanol solutions, the aqueous revealed the presence of saponins. An acute toxicity study in mice showed that the aqueous extract of Picralima nitida would be slightly toxic with a lethal dose (LD) 50 % of 9120.11 mg/kg of body weight (bw). This extract, in rabbits induced a dose-dependent hypotension for the doses between 3.10 -6 g / kg bw and 2.10 -5 g/kg bw with an effective dose 50% (ED50) equal to 4.07×10 -6 g/kg bw. In the presence of atropine (6.10 -9 g/kg), a competitive inhibitor of acetylcholine, the hypotensive effect of aqueous extract of Picralima nitida is reduced, confirming in this extract the presence of cholinomimetics substances of muscarinic type. The results therefore suggest the presence of cholinomimetics substances in the aqueous extract of Picralima nitida seed. These substances could be responsible for the hypotensive effect of this extract. The same extract did not induce diuresis in rats.
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