The Effects of the β2-Adrenergic Receptor Gene Polymorphism on theRisk of Essential Hypertension

Background and Objectives：Considering the physiological importance of the β2-adrenergic receptor (ADRB2) gene, "functional" molecular variations of the gene might cause attenuated vasodilatation, leading to increased total peripheral resistance and; hence, ultimately result in hypertension. Significant evidence has been provided for the pathophysiological involvement of the β2-adrenergic receptor (ADRB2) in hypertension. The genetic variation of the ADRB2 gene, to see if there might be any relationship to essential hypertension, was investigated. Subjects and Methods：One ADRB2 gene polymorphism, Arg16Gly (Arg→Gly variant), was investigated in this study. The genotypes of Arg16Gly in 318 hypertensive patients and 309 normotensive subjects were analyzed. Results：No significant differences were found in the allele and genotype frequencies between patients with hypertension and normotensive subjects. There was no association of the ADRB2 polymorphism (Arg16Gly) with hypertension or the other phenotypes measured in our study populations. Conclusion：Our data suggest that ADRB2 Arg16Gly polymorphisms are unlikely to confer the genetic susceptibility for hypertension in the Korean population. However, further investigation is warranted to clarify the relevance of ADRB2 polymorphisms in blood pressure regulation.ope

Local increase in microparticles from the aspirate of culprit coronary arteries in patients with ST-segment elevation myocardial infarction

OBJECTIVE: It has been reported that the levels of procoagulant microparticles (MPs) are increased in patients with acute coronary syndromes and this may contribute to the formation of intracoronary thrombi. In the current study, we investigated the presence of locally elevated MPs within the culprit coronary arteries of patients with ST-segment elevation myocardial infarction (STEMI). METHODS: The study population consisted of 45 patients with STEMI who underwent primary percutaneous coronary intervention (PCI), and 16 control patients. Before and after PCI, blood samples were collected from the femoral artery and from the culprit coronary arteries. In controls, only peripheral blood was obtained. MPs were measured by a solid-phase capture assay using a commercial kit. The cell origins of MPs were determined by antigenic capture with specific antibodies. RESULTS: Baseline levels of MPs in patients with STEMI were higher than in controls. Before PCI, the levels of MPs were significantly higher in culprit coronary arteries than in peripheral arteries in STEMI patients (20.7 ± 15.5 vs. 14.6 ± 15.4 nM phosphatidylserine (PS) equivalent, p = 0.027). MPs from the culprit coronary artery were significantly reduced after PCI (20.7 ± 15.5 vs. 14.3 ± 14.9 nM PS equivalent, p = 0.010). Similarly, the locally increased levels of endothelial- and platelet-derived MPs within the culprit coronary arteries were significantly decreased after PCI. CONCLUSION: Locally increased levels of MPs in culprit coronary arteries and their significant reduction after successful PCI suggest a potential role in coronary atherothrombosis in the early period of STEMI.ope