L-002 ADENOSINE A2a RECEPTOR GENE EXPRESSION IN ESSENTIAL HYPERTENSION

Abstract

Background Adenosine A2A receptor (ADORA2A) signalling pathway induced vasodilation may have a role in essential hypertension (EH). The study aimed to investigate the expression of ADORA2A in human blood associated with EH. This could provide new insights into potential development of more selective drugs targeting ADORA2A. Methods The 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 ±5 years, gender and ethnicity. Electrocardiography (ECG) was taken in a supine position. Blood samples were collected using the PAXgene blood RNA system. ADORA2A 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 ± 2 years old and their blood pressure were 126 ± 4/82 ± 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, the electrocardiographic left ventricle mass data were similar between groups. The expression level of ADORA2A was measured in blood samples of the HT group compared with the NT group. The amplification efficiency was determined using a 10-fold serial dilution of pooled blood cDNA (r2 = 0.99). The amplification efficiency of the 18 s rRNA and ACTB were 1.95 and 1.94 respectively, whereas the efficiency of ADORA2A was about 2. RT-PCR results indicated relative expression of ADORA2A in the HT group was not significantly different to the NT group (p > 0.05). Conclusion The relative expression level of ADORA2Ain the NT group was not significantly different to the HT group. These subjects were treated with hypertensive agents and blood pressure was within normal range. Further study will investigate expression levels of ADORA2A in untreated hypertensive subjects.