AGTR1 A1166C gene polymorphism is associated with the effectiveness of valsartan monotherapy in Chinese patients with essential hypertension:A retrospective analysis

Objective:To investigate whether angiotensinⅡtype 1 receptor(AGTR1 A1166C)gene polymorphism was associated with the effectiveness of valsartan monotherapy in Chinese patients with essential hypertension.Methods:This retrospective analysis included 198 patients(≥18 years of age)who received valsartan monotherapy(80 mg/day)for newly developed essential hypertension at the authors’center between January 1,2020 and December 31,2023.Genotyping for AGTR1 A1166C gene polymorphism was done by polymerase chain reaction(PCR)-melting curve analysis of genomic DNA from peripheral blood samples.A dominant genetic model for AGTR1 A1166C(AA genotype versus AC+CC genotype)was used.Multivariate regression analysis of baseline variables and AGTR1 polymorphism was conducted to identify predictors of target blood pressure attainment(<140/90 mmHg)at the 4-week follow-up.Results:The median age of the 198 patients was(53.7±13.5)years,and 58%were men.Genotyping assays showed that 164 patients had the AA genotype,and 34 patients were of the AC/CC genotype,including 30 with the AC genotype and 4 with the CC genotype.Allele distribution was consistent with Hardy Weinberg equilibrium.109 Patients(55.1%)attained the blood pressure target.Multivariate analysis showed that smoking(versus no smoking,HR 0.314,95%CI 0.159-0.619,P=0.001)and AGTR1 A1166C AA genotype(versus AC/CC,HR 2.927,95%CI 1.296-6.611,P=0.023)were significant and independent predictors of target attainment.25 Patients(73.5%)with AGTR1 A1166C AC/CC genotype attained the target versus 51.2%(51/164)of patients with AGTR1 A1166C AA genotype(P=0.017).Patients with AGTR1 A1166C AC/CC genotype had a significantly greater reduction in systolic blood pressure[(33.1±10.8)mmHg versus(29.2±11.7)mmHg in AA carriers;(P=0.029)].Conclusions:Hypertensive patients carrying one or two C alleles of the AGTR1 A1166C gene were more responsive to valsartan treatment.

Effects of autoantibodies against AT1-receptor and angiotensin Ⅱ on refractory hypertension

Objective The study will explore effects of the autoantibodies against AT1 receptor and angiotensin Ⅱ on the refractory hypertension. Methods Seventy-seven patients (46 men and 31 women) with essential hypertension were divided into groups of refractory hypertension (RH) and hypertension (HT) according to the 1999 WHO-ISH Guidelines for the Management of Hypertension. Forty normotensives (22 men) were recruited as controls. The mean age was 54. 3±13 years old in RH group, 53. 5±9 years old in HT group and 51. 2±11. 9 years old in normotensives (NT) group. The mean blood pressure was 154. 2±9. 4/98. 4± 8. 2 mmHg in RH group and 130. 1±7. 6/80. 5±6. 7 mmHg in HT group after combination drug therapy of hypertension for 4 weeks. Blood pressure in NT group was 120. 8±11. 7/76. 4 ± 7. 2 mmHg. The epitope of the 2nd extracellular loops of AT1 receptor was synthesized and used as antigens to screen the autoantibodies by ELISA. Plasma angiotensin (Ang) II were examined by a radioimmunoassay. Results The autoantibodies against AT1 receptor were positive in 18 (46. 15 %) patients with RH, in 4 (10. 5 % ) hypertension and in 3 (7. 5 % ) normotensives, P < 0. 01. Ang Ⅱwas 57. 01±52. 63 pmol/L in patients with RH. Both the autoantibodies positive and the Ang Ⅱ increasing were 4 (10. 3 % ) cases, both normal were 7 (17. 9 % ) cases, the autoantibodies positive or Ang II increasing was all of 14 (35. 9 % ) cases (x2 = 0. 09, P>0. 05) . There was no relationship between the autoantibodies against AT1 receptor and the angiotensin Ⅱ in refractory hypertension. Conclusion The autoantibodies against AT1 receptor and Ang Ⅱ might be two independent factors in developing of refractory hypertension. The findings suggest that AT1 receptor an-tagnist used in the treatment of refractory hypertension might have an important value.

AngiotensinⅡor epinephrine hemodynamic and metabolic responses in the liver of L-NAME induced hypertension and spontaneous hypertensive rats

AIM To study hepatic vasoconstriction and glucose release induced by angiotensin(Ang)Ⅱ or Epi in rats with pharmacological hypertension and spontaneously hypertensive rat(SHR).METHODS Isolated liver perfusion was performed following portal vein and vena cava cannulation; AngⅡ or epinephrine(Epi) was injected in bolus and portal pressure monitored; glucose release was measured in perfusate aliquots. RESULTS The portal hypertensive response(PHR) and the glucose release induced by AngⅡ of L-NAME were similar to normal rats(WIS). On the other hand, the PHR inducedby Epi in L-NAME was higher whereas the glucose release was lower compared to WIS. Despite the similar glycogen content, glucose release induced by AngⅡ was lower in SHR compared to Wistar-Kyoto rats although both PHR and glucose release induced by Epi in were similar. CONCLUSION AngⅡ and Epi responses are altered in different ways in these hypertension models. Our results suggest that inhibition of NO production seems to be involved in the hepatic effects induced by Epi but not by AngⅡ; the diminished glucose release induced by AngⅡ in SHR is not related to glycogen content.

The changes of serum nitric oxide, angiotensin Ⅱ and superoxide anion in renal artery hypertension rat

Objectives To study the changes of nitric oxide, angiotensin Ⅱ and superoxide anion in renal artery hypertension pathogenesis. Methods Male Wistar rats weighing 256 -285g were divided into 5 groups randomly, 10 rats of each group. Control group: false operation was made and routine diet was given; Ligature group: left renal artery was ligatured uncompletely and routine diet was given; Ligature + Losartan group: left renal artery was ligatured uneompletely and Losartan 20mg · kg^(-1) · d^(-1) was added in the drinking water; Ligature + L -Arg group: left renal artery was ligatured uncompletely and L -Arg 2g · kg^(-1) · d^(-1) was added in the drinking water; Ligature + L - Arg + Losartan group: left renal artery was ligatured uncompletely and L - Arg 2g· kg^(-1)· d^(-1) and Losartan 20mg · kg^(-1)· d^(-1) was added in the drinking water. Blood pressure and heart rate were measured before and at the end of the experiment. One week after ligature, blood was drawn to determine angiotensin Ⅱ, cGMP, nitric oxide, nitric oxide synthase (NOS), O_2^-, superoxide dismutase (SOD). Results Systolic blood pressure was higher in ligature group than that in control group (p <0.05), systolic blood pressure was much lower in ligature + Losartan group than that in ligature group. Heart rate did not change significantly after experiment (p > 0. 05). AngⅡ was higher in ligature group than that in control group, even much higher in ligature + Losartan group (p < 0. 01 ). There was no difference of cGMP in each group (p >. 05). The concentration of NO was lower in ligature group (p <0.05), NO was higher in ligature + L - Arg + Losartan group than that in ligature group (p <0.05). O_2^- was higher in ligature group and ligature + L - Arg group than that in control group (p < 0. 05), O_2^- was lower in ligature + Losartan group than that in ligature group (p <0. 05). The level of SOD was lower in ligature group than that in control group (p <0.05), higher in ligature + L- Arg group and ligature + L - Arg + Losartan group than that in ligature group (p <0. 05). Conclusions AngⅡ,O_2^- and NO imbalance play an important role in hypertension pathogenesis, LArg and losartan may have protective effect.

A Quantitative Study on Vascular Angiotensin Ⅱ Receptors in Rats with Portal Hypertension

Angiotension-Ⅱ(A-Ⅱ) receptor maximal binding capacity (Bmax) and dissociation constants (Kd) of different blood vessels in rats with prehepatic portal hypertension were studied by radioligand binding analysis. The results showed that the A-Ⅱreceptor Bmax. in the thoracic aorta, superior mesenteric artery and portal vein of portal hypertensive animals (113. 7±19. 4 fmol/mg protein, 206.9 ±39. 3 fmol/mg protein and 31. 5±9. 2 fmol/mg protein respectively ) was all significantly lower than that of controls (146. 8±24. 5 fmol/mg protein, 297. 2±44. 7 fmol/mg protein and 53. 4±12.1 fmol/mg protein respectively, P＜0. 01).The A-Ⅱ receptor Kd in the superior mesenteric artery was markedly increased in portal hypertensive animals (1. 03±0.11 nmol/L) compared with that in controls (0. 88±0. 08 nmol/L, P＜0. 05). In the thoracic aorta and portal vein, the A-Ⅱ receptor Kd in portal hypertensive animals was slightly higher than that in controls, but no significant difference was observed between the two groups. The results suggested that the vascular hyporesponsiveness to A-Ⅱ in portal hypertension was caused partially by a reduction in number and a decrease in affinity of vascular A- Ⅱ receptors, and these changes might possibly lead to the formation of hyperdynamic circulation.

SUPPRESSION OF ANGⅡ AFTER ACUTE SALINE LOAD ASSOCIATED WITH THE CHANGES OF PLASMA ANP AND SODIUM METABOLISM IN SALT-SENSITIVE HYPERTENSION PATIENTS

Objective To observe the changes of plasma AngⅡ,ANP and their relationship with urine sodium excretion in salt sensitive hypertension. Methods The salt sensitivity was determined by acute saline loading test in 173 primary hypertensives of Stage Ⅰ or Stage Ⅱ. Plasma AngⅡand ANP was determined by radioimmunoassay. Results After acute salt load, AngⅡ was suppressed inadequately. The plasma ANP secretion was not increased. The urine sodiun excretion was delayed, Na + in RBC was increased in salt sensitive subjects. The plasma ANP was decreased in the salt sensitive subjects without AngⅡ suppressed. The 24 hours urine sodium excretion was lower than those AngⅡ suppressed.Conclusion The changes of plasma RAS are not homogeneous after salt load. Those without the plasma AngⅡ suppressed have more severe sodium metabolism abnormalities and the endogenous ANP secretion is impaired in salt sensitive patients.

Combined effects of hypertension and angiotensin Ⅱ on the risk of coronary heart disease:a population-based prospective cohort study among Inner Mongolians in China

Objective To investigate the combined effects of hypertension and angiotensinⅡon the risk of coronary heart disease(CHD)on the basis of a 10-year prospective study in an Inner Mongolian population of China.Methods Based on a cross-sectional survey,a prospective cohort study was conducted from June 2003 to July 2012 among 2,530 Mongolian people.

Effects of IGF-Ⅱand TGF-β1 on invasiveness of placental trophoblast cells in patients with pregnancy-induced hypertension syndrome

Objective: This study was to investigate the invasiveness of pregnancy-induced hypertension (PIH) trophoblast cells and evaluate the effects of IGF-Ⅱand TGF-β1 on cytotrophoblast invasion.Methods: Cytotrophoblast cells from normal and PIH placenta were separated and purified. Cytotrophoblast invasiveness of normal and PIH placenta was measured by in vitro invasion assay. Effects of IGF-Ⅱand TGF-β1 on cytotrophoblast invasion were also studied.Results: In PIH group, cytotrophoblast invasiveness was dramatically decreased. In normal group, trophoblast invasiveness was significantly enhanced by IGF-Ⅱ but inhibited by TGF-β1. Neither IGF-Ⅱ nor TGF-β1 had statistically significant effects on PIH trophoblast invasion.Conclusions: PIH cytotrophoblast invasiveness dramatically decreases as compared to the normal level. IGF-Ⅱand TGF-β1 may play an important role in shallow trophoblast invasion on PIH.

Salvianolic acid A attenuates vascular remodeling in a pulmonary arterial hypertension rat model

OBJECTIVE The current therapeutic approaches have a limited effect on the dysregulated pulmonary vascular remodeling,which is characteristic of pulmonary arterial hypertension(PAH).In this study we exam-ined whether salvianolic acid A(SAA)extracted from the traditional Chinese medicine′Dan Shen′attenuated vascular remodeling in a PAH rat model,and elucidated the underlying mechanisms.METHODS PAH was induced in rats by injecting a single dose of monocrotaline(MCT 60 mg·kg-1,sc).The rats were orally treated with either SAA(0.3,1,3 mg·kg-1·d-1)or a positive control bosentan(30 mg·kg-1·d-1)for 4 weeks.Echocardiography and hemodynamic measurements were performed on d 28.Then the hearts and lungs were harvested,the organ indices and pulmonary artery wall thickness were calculated,and biochemical and histochemical analysis were conducted.The levels of apoptotic and signaling proteins in the lungs were measured using immunoblotting.RESULTS Treatment with SAA or bosentan effectively ameliorated MCTinduced pulmonary artery remodeling,pulmonary hemodynamic abnormalities and the subsequent increases of right ventricular systolic pressure(RVSP).Furthermore,the treatments significantly attenuated MCT-induced hypertrophic damage of myocardium,parenchymal injury and collagen deposition in the lungs.Moreover,the treatments attenuated MCT-induced apoptosis and fibrosis in the lungs.The treatments partially restored MCT-induced reductions of bone morphogenetic protein typeⅡreceptor(BMPRⅡ)and phosphorylated Smad1/5 in the lungs.CONCLUSION SAA ameliorates the pulmonary arterial remodeling in MCT-induced PAH rats most likely via activating the BMPRⅡ-Smad pathway and inhibiting apoptosis.Thus,SAA may have therapeutic potential for the patients at high risk of PAH.

Altered Erythrocyte Membrane Calcium Binding in Hypertensive Rats and the Effects of Sodium Tanshinone Ⅱ-A Sulphonate on It

The calcium binding of erythrocyte membrane was determined in spontaneous hypertensiverats (SHR)and renovascular hypertensive rats (RVHR two-kidney, one-clip model) and the effect ofsodium tanshinone Ⅱ-A sulfonate(DS-201)on the calcium binding in SHRs was investigated. Ourresults show that the basal calcium binding was reduced in SHRs (P<0.01 vs WKY),while the maximalcalcium binding was not,but both typies calcium bindings had no significant change in RVHRs.Sodiumtanshinone Ⅱ-A sulfonate (125μ mol/L)have no effect on the calcium binding of ecythrocyte membraneof SHR in vitro.These data further support the hypothesis that there is a cell membrane abnormalitypresent in SHRs which may possibly serve as a marker genetics of in hypertension.

Induction of tissue angiotensin Ⅱ-forming activity in two-kidney, one-clip hypertensive hamster model

AIM: To evaluate the role of chymase in blood pressure regulation and its actions on tissue renin-angiotensin system.METHODS: A two-kidney, one-clip(2K1C) hypertension model was developed in Syrian hamsters, which have a human-type chymase. Either an angiotensin(Ang) converting enzyme(ACE) inhibitor(ACE-I; temocapril, 30 mg/kg per day), Ang Ⅱ type 1 receptor antagonist(ARB; CS866, 10 mg/kg per day), or vehicle was administered, beginning 2 wk after renal artery clipping and continued for 16 wk. At the end of this protocol, hearts, aortas, and lungs were removed, and total Ang Ⅱ-forming activities and ACE- and chymasedependent Ang Ⅱ-forming activities were determined.RESULTS: After renal artery clipping, systolic blood pressure in the vehicle group was significantly higher compared with that in a sham-operated group throughoutthe experimental period. Both ACE-I and ARB treatments revealed similar antihypertensive effects. Moreover, in the vehicle group, cardiac total and chymase-dependent Ang Ⅱ-forming activities significantly increased at 18 wk after clipping. Further, cardiac total and chymase-dependent Ang Ⅱ-forming activities decreased significantly after ACE-I or ARB treatment for 16 wk. In addition, chymase-dependent Ang Ⅱ-forming activity significantly increased in the aorta, although these changes were inhibited only by ARB. ARB treatment was more effective compared with ACE-I treatment in reversing the changes in tissue Ang Ⅱ formation, particularly in the aorta, despite their similar antihypertensive effects.CONCLUSION: Chymase does not play a major role in maintaining blood pressure and tissue ACE and chymase are regulated in a tissue-dependent manner in 2K1 C hamster.

Brain inflammation in neurogenic hypertension

One likely mechanism of essential hypertension(EH) is increased sympathoexcitation due to abnormal functions in the cardiovascular center of the brain. Recent findings obtained using experimental animal models of EH have shown that abnormal inflammation in the cardiovascular center may contribute to the onset of hypertension. Inflammatory molecules such as cytokines and reactive oxygen species released from the inflamed vasculature and glial cells in the medulla oblongata and hypothalamus might directly or indirectly affect neuronal functions. This in turn could increase sympathetic nerve activity and consequently arterial pressure. Abnormal inflammatory responses in the brain could also be central mechanisms underlying angiotensin Ⅱ-related EH. In this review, we present the current understanding of EH mechanisms with regard to inflammatory responses in the cardiovascular center.

ANGIOTENSIN Ⅱ IMMUNOREACTIVITIES IN CARDIOVASCULAR BRAIN AREAS OF DEVELOPING SPONTANEOUSLY HYPERTENSIVE AND NORMOTENSIVE WISTAR KYOTO RATS:AGE-AND SEX-RELATED DIFFERENCES

Angiotensin Ⅱ immunoreactivity (ir-Ang Ⅱ) was measured in brain areas,known to be involved in the control of circulation, in spontaneously hypertensive rats(SHR) and normotensive, Wistar Kyoto rats as controls (WKY) of 1-]2 weeks old and of both sexes. The systolic pressure (SP), in rats of 4-12 weeks old,increased with age and was signifficantly higher in SHR than WKY. In SHR, the increase was also significantly greater in male than female. The ir-Ang Ⅱ increased with age in all cardiovascular brain areas up to 12 weeks old in SHR, but only up to 4 weeks old in WKY. There was also sex difference in SHR. The changes in ir-Ang Ⅱ, particularly in the ventrolateral medulla (VLM), correlated well with changes in SP. The findings suggest thal interaction between brain Ang Ⅱ and cardiovascular brain areas, particularly the VLM and hypothalamus, may be crucial in the development of hypertension. The results also indicale sexual dimorphism in brain Ang Ⅱ in addition to blood pressure reaction in the developing SHR.

应用动态血压监测仪及人体成分分析仪观察氨氯地平贝那普利片(Ⅱ)对原发性高血压患者的疗效

目的 评价动态血压监测仪及人体成分分析仪在氨氯地平贝那普利片(Ⅱ)治疗原发性高血压患者疗效中的作用。方法 110例原发性高血压患者,入组前停用既往所有降压药,洗脱期间,饮食方式不变。2周之后接受氨氯地平贝那普利片(Ⅱ)治疗,监测并比较患者治疗前后动态血压参数(白天、夜间、24 h的收缩压和舒张压)、平滑指数、人体成分[骨骼肌质量、脂肪含量、骨骼肌质量指数(SMI)]。结果 治疗后,白天、夜间、24 h的收缩压分别为(132.58±11.22)、(120.23±12.83)、(126.10±8.11)mm Hg(1 mm Hg=0.133 kPa),均低于治疗前的(148.36±10.42)、(133.11±12.91)、(142.26±10.15)mm Hg,舒张压分别为(75.65±11.96)、(68.31±9.10)、(71.40±8.70)mm Hg,均低于治疗前的(85.03±10.98)、(77.85±10.84)、(83.92±9.89)mm Hg,治疗后的平滑指数(2.00±0.23)高于治疗前的(1.21±0.26),差异具有统计学意义(P<0.01)。患者治疗后的骨骼肌质量(35.75±6.84)kg、SMI(8.38±0.51)kg/m2均高于治疗前的(25.15±6.58)kg、(7.95±0.44)kg/m2,脂肪含量(18.83±4.15)kg低于治疗前的(23.12±4.51)kg,差异具有统计学意义(P<0.01)。结论 氨氯地平贝那普利片(Ⅱ)能有效平稳地降低原发性高血压患者的动态血压,且增加骨骼肌质量、降低脂肪含量,优化人体成分,值得临床推广。

POLYMORPHISM OF ANGIOTENSIN I TYPE 1 RECEPTOR GENE IN ELDERLY PATIENTS WITH ESSENTIAL HYPERTENSION

Objective To detect the A/C1165 polymorphism of angiotensin Ⅱ type Ⅰ receptor (AT1-R)gene in essential hypertensive elderly. Methods The A/C1166 polymorphism of AT1-R gene was assessed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) in a case-control study of 87 essential hypertensive elders (EH) and 55 normolensive elders (NT). Results The genotype frequencies of AA, AC, CC were 0 .805 , 0.161, 0 .034 in EH group and 0 .927 ,0 .073 ,0 .000 in NT group respectively. The frequency of C61166 allele was higher in EH group (0.115) than in NT group (0 .036 )(P<0 .05 ). Conclusion The resultsindicate that A/C1166 polymorphism of AT1-R gene may be associated with essential hypertension in elderly.

妊娠高血压患者血管紧张素Ⅱ及AT1R、AT2R的表达及意义

目的:探讨妊娠高血压(HDCP)患者血管紧张素Ⅱ(AngⅡ)及AngⅡ受体-1(AT1R)和AngⅡ受体-2(AT2R)的表达及意义。方法:选取2021年1月—2022月年9月孝感市中心医院收治的90例HDCP患者作为观察组,并将观察组根据病情程度分为HDCP组、轻度子痫前期组和重度子痫前期组3个亚组,将同期产检的90例健康孕妇作为对照组。检测并比较观察组与对照组、观察组不同亚组AngⅡ水平、AT1R和AT2R阳性表达情况。结果:观察组产前母血、产后脐血AngⅡ水平低于对照组,产后母血AngⅡ水平、AT1R、AT2R总阳性率高于对照组,差异有统计学意义(P<0.05)。不同病情程度HDCP患者产前母血、产后脐血AngⅡ水平比较,HDCP组>轻度子痫前期组>重度子痫前期组;不同病情程度HDCP患者产后母血AngⅡ水平比较,HDCP组<轻度子痫前期组<重度子痫前期组;不同病情程度HDCP患者AT1R、AT2R阳性情况比较,HDCP组<轻度子痫前期组<重度子痫前期组,差异有统计学意义(P<0.05)。结论:HDCP患者母血、脐血AngⅡ存在异常表达,其AT1R、AT2R阳性率随病情加重而升高,检测上述指标有助于为HDCP发病机制、早期诊断与治疗提供参考。

血清STNFR-Ⅱ、KIM-1、β2-MG水平与妊娠期高血压疾病患者早期肾损伤的相关性分析

目的分析血清STNFR-Ⅱ、KIM-1、β2-MG水平与妊娠期高血压疾病患者早期肾损伤的相关性。方法选取我院2021年2月至2023年11月收治的100例妊娠期高血压疾病患者纳入研究组,另选取同期我院100例健康妊娠期女性纳入参照组。比较研究组和参照组以及研究组中合并与未合并早期肾损伤患者的血清STNFR-Ⅱ、KIM-1、β2-MG水平,并分析血清STNFR-Ⅱ、KIM-1、β2-MG水平与妊娠期高血压患者发生早期肾损伤的相关性。结果研究组血清STNFR-Ⅱ、KIM-1、β2-MG水平高于参照组(P<0.05)。研究组中合并早期肾损伤患者的血清STNFR-Ⅱ、KIM-1、β2-MG水平高于未合并早期肾损伤患者(P<0.05)。Spearman相关性分析结果显示,血清STNFR-Ⅱ、KIM-1、β2-MG水平与妊娠期高血压疾病患者早期肾损伤呈明显正相关(r=0.621、0.583、0.604,P=0.000、0.000、0.000)。结论血清STNFR-Ⅱ、KIM-1、β2-MG水平与妊娠期高血压疾病患者发生早期肾损伤关系密切,临床可通过检测妊娠期高血压疾病患者血清STNFR-Ⅱ、KIM-1、β2-MG水平评估其是否发生早期肾损伤。

血管内皮素和血管紧张素Ⅱ释放的相互关系

为探讨血管内皮素(ET)和血管紧张素Ⅱ(AⅡ)释放的相互关系,本工作用放射免疫方法测定离体灌流大鼠主动脉的ET和AⅡ的释放,发现EF或AⅡ呈剂量依赖地促进主动脉条释放AⅡ或EF。缺氧可显著地促进ET和AⅡ的释放,而ET或AⅡ抗血清明显地抑制缺氧所致的AⅡ或ET的释放。临床观察发现血管紧张素转换酶抑制剂—巯甲丙脯酸治疗原发性高血压,有效地降低病人血浆ET水平。结果提示:血管AⅡ和ET的释放间存在着相互促进的正反馈关系。

针刺仿真手法对高血压大鼠血压及心肌血管紧张素Ⅱ的影响

目的:通过针刺手法仿真系统,以不同刺激量参数的捻转手法刺激自发性高血压大鼠(SHR),比较其降压效应及对心肌血管紧张素(Ang)Ⅱ含量的影响,为针灸治疗高血压临床研究探索最佳针刺刺激参数,同时为针刺手法量化和规范化研究提供思路。方法:33只SHR随机分为轻刺激组(n=8)、中刺激组(n=8)、重刺激组(n=8)、模型组(n=9),另设8只正常动物组。采用PowerLab无创尾动脉血压测定分析系统对大鼠进行血压测定,并应用放射免疫法检测各组大鼠心肌组织AngⅡ含量的变化。轻、中、重3种刺激参数旋转角度和频率分别为:144°、75次/min,255°、111次/min,360°、140次/min。结果:轻刺激量捻转手法与中刺激量捻转手法均有显著抑制血压上升的作用(P<0.01),而重刺激量捻转手法抑制血压上升的效果不明显(P>0.05),SHR模型组的血压3周后显著升高(P<0.01)。同时发现,各治疗组大鼠心肌组织中的AngⅡ水平仍高于正常组(P<0.05),与模型组的差异无显著性意义(P>0.05)。结论:不同量化参数的捻转手法的针刺效应具有差异性,针刺治疗的效果与手法参数的量化有密切的关系;本研究同时提示针刺治疗高血压可能与AngⅡ无明显相关性,其机制有待于进一步研究。

血浆Apelin、血管紧张素Ⅱ与高血压及早期肾损害的相关性研究

目的:探讨一种新的血管活性肽血浆Apelin和血管紧张素Ⅱ(Ang Ⅱ)水平在高血压时的改变及其与高血压早期肾损害的关系,为Apelin成为高血压可能的治疗靶点提供临床研究数据。方法:研究对象来源于社区人群的横断面调查,入选标准为年龄30岁以上,居住当地≥5年的常住居民,共纳入671例,其中高血压组317例,非高血压组354例。所有研究对象进行Apelin、Ang Ⅱ、尿肌酐和尿白蛋白等检测。Pearson相关分析及多元线性回归分析血压、尿白蛋白与尿肌酐比值(UACR)与Apelin和Ang Ⅱ的关系。结果:高血压组的Apelin水平低于非高血压组(P<0.01),Ang Ⅱ和UACR水平高于非高血压组(P<0.01);平均动脉压与Ln(Apelin)存在负相关(P<0.01),与Ln(Ang Ⅱ)存在正相关(P<0.01),此相关性在调整性别、年龄和血脂等影响因素后仍存在;Ln(Apelin)与Ln(Ang Ⅱ)存在负相关(P<0.01),此相关性在调整了年龄、性别、血压和血脂等混杂因素后仍然存在;在高血压组,合并早期肾损害者的Apelin水平偏低(P<0.05),Ang Ⅱ水平偏高(P<0.05)。相关性分析显示Ln(UACR)与Ln(Apelin)存在负相关(P<0.01),与Ln(Ang Ⅱ)存在正相关(P<0.01),此相关性在调整了性别、年龄、平均动脉压和血脂等混杂因素后仍存在。结论:高血压及高血压早期肾损害人群Apelin水平下降,Apelin与Ang Ⅱ存在负相关关系。