The Research Of NADPH Oxidase And Subclinical Target Organ Damage About Primary Hypertension In Patients

BackgroundPrimary hypertension is an important cause or a risk factor of a variety ofcardiovascular and cerebrovascular diseases. The target organ damages influence thestructure and function of some important organs such as heart, brain, kidney andperipheral vascular. The subclinical target organ damage refers to the early stage ofdamage that high blood pressure bring to heart, brain, kidney and peripheral vascular,which have not resulted in clinical symptoms. The research proves that hypertensiontarget organ damage is closely related to the bad prognosis and cardiovascular eventsof high blood pressure patients, but pathological mechanism still is not very clear,therefore, the further research the related mechanism of the hypertension subclinicaltarget organ damage has a very important clinical significance. The mechanism ofhypertension subclinical target organ damage is now thought in addition related to theblood pressure level itself,and still related to endothelial activation, platelet activation,renin angiotensin system activation and oxidative stress and so on.At present, the study about oxidative stress in hypertension target organ damage,especially in the subclinical target organ damage of the function and mechanism isvery little. An important sign of oxidative stress is the increasing of body reactiveoxygen species (ROS), nicotinamide adenine dinucleotide phosphate oxidase(NADPH oxidase) is the most main catalytic enzymes of ROS. The study about thefunction and mechanism of NADPH oxidase in hypertension subclinical targetorgan damage, and the discusses the effect of oxidative stress in early hypertensiontarget organ damage will provide the evidence for hypertension prognosis assessmentand early intervention. ObjectiveThrough detecting the level of NADPH oxidase, MDA and angiotensin II inpatients’ peripheral blood with hypertension subclinical target organ damage, thisstudy aims to analysis the correlation between the level of NADPH oxidase and someother factors such as age, body mass index, smoking index, lipids, uric acid ofhypertension patients, and also to discuss the function and mechanism of oxidativestress in hypertension subclinical target organ damage.MethodsChoose116patients with the subclinical target-organ damage from whom withprimary hypertension from March2010to December2011in Changsha CentralHospital as the research objects (experimental group), and84patients without anytarget organs damage as control group. The clinical target organ damage assessmentstandards are according to the appearing of one or more than one indexl:①leftventricular hypertrophy,②the abnormal carotid intima-media thickening or plaqueformation,③the appearance of microalbuminuria. In the study, all patients werecollected blood in the early morning with an empty stomach(fasting8h above), andthen were used to detect the level of blood sugar, lipids (TC, TG, LDL-C, HDL-C),and renal level. The research uses ELISA to detect the level of plasma angiotensin II(AngII), NADPH oxidase and malondialdehyde (MDA).Results(1) In116cases, the patients who with subclinical target organ damage(experimental group) have only one organ damaged are (54,46.6%);those who havetwo organs damaged are (36,31%); and those who have three organs damaged are(26,22.4%).(2) Compared to the primary hypertension patients with no target organ damage(control group), the difference was not statistically significant from the patients withthe target organ damage clinical patients (experimental group) in the sex, course ofdisease, diastolic blood pressure, fasting blood sugar, triglyceride level (p>0.05);Experimental group in age (67.17±6.95) years, systolic blood pressure (155.86±10.94) mmHg, body mass index（25.13±2.54）kg/m~2, smoking index（516.5±291.09）, totalcholesterol（4.83±0.61）mmol/L, low density lipoprotein cholesterol（2.98±0.66）mmol/L,and uric acid（343.33±56.9）μmol/L were significantly higher than controls in（age (64.69±8.34) years，systolic blood pressure (148.82±10.97)mmHg，bodymass index (22.04±3.22) kg/m~2，smoking index (314.29±262.62)，total cholesterol（4.53±0.81）mmol/L，low density lipoprotein cholesterol (2.61±0.89) mmol/L anduric acid (298.55±67.75) μmol/L）(p <0.05).(3) The NADPH oxidase expression level in experimental group [(6.08±3.01)U/mL]was significantly higher than controls [(4.21±2.31) U/mL](p <0.05).;the MDA expression level in experimental group [(6.99±4.42) mmol/L] wassignificantly higher than controls [(5.07±2.42)mmol/L](p <0.05); the plasma AngIIexpression level in experimental group[(130.24±83.04)ng/L]was significantly higherthan controls [(96.64±59.55)ng/L](p <0.05).(4) The NADPH expression level in experimental group patients are positivelycorrelated to oxidase AngII, MDA expression level (r=0.922and0.881, p <0.05).(5) Two groups of patients peripheral blood NADPH oxidase level werepositively correlated to age (r=0.036, p <0.05), smoking index (r=0.164, p <0.05)，body mass index (r=0.272, p <0.05),, uric acid (r=0.283, p <0.05).Conclusion(1) Age, smoking index, systolic blood pressure, body mass indexhypercholesterolemia and hyperuricemia and other are the risk factors of hypertensionsubclinical target organ damage;(2) NADPH oxidase expression level is significantly higher in peripheral bloodof primary hypertension subclinical target organ damage patients l, indicating that theoxidative stress participates in the pathophysiological process of hypertensiontarget-organ damage;(3) Oxidative stress may play an important role in the origin and development ofsubclinical target organ damage by activating the active oxygen pathway ofAngII-NADPH oxidase; (4) The dangerous factors such as age, smoking index, body mass index maypromote early target organ damage in primary hypertension by activating NADPHoxidase.