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1.
Angiotensin-II stimulates nitric oxide release in isolated perfused renal resistance arteries 总被引:3,自引:0,他引:3
C. Thorup Mark Kornfeld Joseph M. Winaver Michael S. Goligorsky Leon C. Moore 《Pflügers Archiv : European journal of physiology》1998,435(3):432-434
Nitric oxide (NO) has been implicated as a modulator of the vascular effects of angiotensin II (ANG II) in the kidney. We
used a NO-sensitive microelectrode to study the effect of ANG II on NO release, and to determine the effect of selective inhibition
of the ANG II subtype I receptor (AT1) with losartan (LOS) and candesartan (CAN). NO release from isolated and perfused renal
resistance arteries was measured with a porphyrin-electroplated, carbon fiber. The vessels were microdissected from isolated
perfused rat kidneys and perfused at constant flow and pressure in vitro. The NO-electrode was placed inside the glass collection
cannula to measure vessel effluent NO concentration. ANG II stimulated NO release in a dose-dependent fashion: 0.1 nM, 10 nM
and 1000 nM ANG II increased NO-oxidation current by 85±18 pA (n = 11), 148±22 pA (n = 11), and 193±29 pA (n = 11), respectively. These currents correspond to changes in effluent NO concentration of 3.4±0.5 nM, 6.1±1.1 nM, and 8.2±1.3 nM,
respectively. Neither LOS (1 μM) nor CAN (1 nM) significantly affected basal NO production, but both AT1-receptor blockers
markedly blunted NO release in response to ANG II (10 nM): 77±6% inhibition with LOS (n = 8) and 63±9% with CAN (n = 8). These results are the first to demonstrate that ANG II stimulates NO release in isolated renal resistance arteries,
and that ANG II-induced NO release is blunted by simultaneous AT1-receptor blockade. Our findings suggest that endothelium-dependent
modulation of ANG II-induced vasoconstriction in renal resistance arteries is mediated, at least in part, by AT1-receptor-dependent
NO release.
Received: 24 September 1997 / Accepted: 20 October 1997 相似文献
2.
Pharmacokinetics and pharmacodynamics of candesartan cilexetil in patients with normal to severely impaired renal function 总被引:1,自引:0,他引:1
Buter H Navis GY Woittiez AJ de Zeeuw D de Jong PE 《European journal of clinical pharmacology》1999,54(12):953-958
Objective: We studied the pharmacokinetics and pharmacodynamics of single and multiple doses of candesartan cilexetil 8 mg per day
in hypertensive patients with different degrees of renal function impairment. Candesartan is an angiotensin II subtype 1 (AT1)
receptor antagonist that is administered orally as candesartan cilexetil which is converted in the active compound.
Methods: Twenty-three patients were included, divided into groups according to creatinine clearance (cr cl. group A >60 nl · min−1 · 1.73 m−2, group B 30–60 ml · min−1 · 1.73 m−2 and group C 15–30 ml · min−1 · 1.73 m−2).
Results: Trough serum concentrations of candesartan were higher in group C compared with group A. The values did not increase after
multiple dosing, indicating absence of accumulation. There was a significant negative correlation between the area under the
concentration-time curve extrapolated to time infinity (AUCinf) and the glomerular filtration rate (GFR) indicating a lower renal clearance of candesartan in patients with impaired renal
function. The onset of haemodynamic and hormonal effects was gradual. During the single-dose study blood pressure as well
as plasma renin activity (PRA) and angiotensin II were unchanged at peak. At day 5 of the multiple-dose study blood pressure
was lower and both PRA and angiotensin II were higher compared with baseline.
Conclusion: Although serum trough levels increased during repeated administration and half-life was higher in patients with impaired
renal function, candesartan cilexetil at a dose of 8 mg per day does not lead to drug accumulation in these patients. This
dose is effective in lowering blood pressure and appears to be suitable for patients with renal function impairment.
Received: 3 August 1998 / Accepted in revised form: 19 October 1998 相似文献
3.
4.
目的:制备坎地沙坦酯片并优化处方,并对其进行初步稳定性考察。方法:采用Box-Behnken试验设计,以填充剂配比(X1)、崩解剂(X2,%)和润滑剂(X3,%)用量为影响因素,以片重差异(Y1,%)、脆碎度(Y2,%)、崩解时限(Y3,min)、坎地沙坦酯溶出度(Y4,%)为片剂考察指标,得到最优处方;采用f2相似因子法评价自制制剂和参比制剂在溶出介质中的体外溶出行为。通过高温、高湿、光照试验初步考察制剂稳定性。结果:坎地沙坦酯片的最优处方组成为:填充剂一水乳糖与预交化淀粉比例为7∶1、崩解剂交联羧甲基纤维素钠占片重为5.5%,润滑剂硬脂酸镁占片重为0.5%。自制片剂和参比制剂在4种溶出介质中的累积溶出度相似因子f2分别为60.62,73.34,66.95,68.60。结论:制备的坎地沙坦酯片各项指标均符合规定,工艺稳定可靠。 相似文献
5.
目的观察左旋氨氯地平对阵发性房颤并高血压患者P波离散度(Pd)、左房内径、高敏C反应蛋白(hs—CRP)水平、房颤发作情况的影响。方法将阵发性房颤并高血压患者100例随机分为治疗组(50例)和对照组(50例)。降压药物治疗组给予左旋氨氯地平,对照组给予坎地沙坦,随访1年,观察治疗前后Pd、左房内径、hs—CRP水平及房颤发作情况。结果至随访结束,在长期应用胺碘酮的患者中,对照组房颤复发17例,占81.0%,治疗组房颤复发22例,占95.7%,两组之间差异无统计学意义(x^2=1.122,P〉0.05)。未长期应用胺碘酮的患者,对照组、治疗组在7-12个月时房颤发作次数均较治疗前减少(t=2.823,P〈0.01;t=2.655,P〈0.05),但两组之间差异无统计学意义(t=0.594,P〉0.05)。与治疗前比较,对照组、治疗组的Pd、左房内径、hs—CRP均降低(t=4.025-13.546,P〈0.01),治疗后两组之间Pd、左房内径、hs—CRP比较,差异无统计学意义(t=1.234-1.514,P〉0.05)。结论左旋氨氯地平可减少阵发性房颤并高血压患者房颤的复发,降低Pd、左房内径和hs—CRP水平,其效果与坎地沙坦没有差异。 相似文献
6.
目的探究银杏达莫注射液联合坎地沙坦酯治疗早期糖尿病肾病的临床疗效。方法选取2015年5月—2016年12月在厦门市第五医院进行治疗的236例早期糖尿病肾病,随机分为对照组和治疗组,每组各118例。对照组口服坎地沙坦酯片,1片/次,1次/d。治疗组在对照组治疗基础上静脉滴注银杏达莫注射液,20 m L银杏达莫注射液加入到250 m L生理盐水,1次/d。两组均连续治疗8周。观察两组的临床疗效,同时观察两组治疗前后血肌酐(Scr)、尿素氮(BUN)、24 h尿蛋白(TP/24 h)、总胆固醇(TC)、血流动力学指标的变化情况。结果治疗后,对照组和治疗组的总有效率分别为83.05%、91.53%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者TP/24 h、Scr、BUN、TC、血液黏度、纤维蛋白原均显著降低,同组治疗前后差异有统计学意义(P0.05);治疗后,治疗组TP/24 h、Scr、BUN、TC、血液黏度、红细胞压积、纤维蛋白原低于对照组,两组比较差异具有统计学意义(P0.05)。结论银杏达莫注射液联合坎地沙坦酯治疗糖尿病肾病具有较好的临床疗效,可降低患者尿微量蛋白水平,降低血液黏度,改善肾功能,具有一定的临床推广应用价值。 相似文献
7.
目的 建立测定坎地沙坦酯氨氯地平片有关物质的高效液相色谱法。方法 采用Inertsil ODS-SP C18(150 mm× 4.6 mm,5 μm)色谱柱,以0.035 mol·L-1 KH2PO4(磷酸调pH 3.0)-甲醇-乙腈为流动相,梯度洗脱,检测波长238 nm,流速1.0 mL·min-1。结果 特异性杂质和破坏条件下产生的降解产物与主药分离较好,3批样品最大单个杂质为坎地沙坦酯杂质B,总杂质均〈0.5%。结论 本法专属性强,灵敏度高,重现性好,能够有效控制产品质量。 相似文献
8.
目的:建立测定坎地沙坦酯原料药中8种有机溶剂甲醇、乙醇、乙腈、丙酮、乙醚、二氯甲烷、乙酸乙酯与四氢呋喃残留量的方法。方法:采用气相色谱法。色谱柱为Agilent HP-5毛细管柱,以(5%)苯基-(95%)甲基聚硅氧烷为固定液,柱温采用程序升温,氢火焰离子化检测器温度为250℃;载气为高纯N2;顶空进样,加热温度为100℃,加热时间为30 min。结果:8种有机溶剂在各自的检测质量浓度范围内线性关系良好(r=0.999 60.999 9),平均回收率均为99.6%0.999 9),平均回收率均为99.6%100.3%(RSD=0.89%100.3%(RSD=0.89%1.98%,n=3);定量限分别为0.09、0.15、0.12、0.3、0.6、0.18、0.45、0.21 ng;检测限分别为0.03、0.05、0.04、0.1、0.2、0.06、0.15、0.07 ng。样品中只检出了丙酮。结论:建立的方法操作简便、精密度高,可有效控制坎地沙坦酯原料药中残留的8种有机溶剂。 相似文献
9.
10.
目的探究阿托伐他汀联合坎地沙坦酯治疗原发性高血压的临床疗效。方法选取2012年1月—2014年11月义马煤业集团股份有限公司收治的原发性高血压患者300例,随机分为对照组和治疗组,每组150例。对照组口服坎地沙坦酯片,2片/次,1次/d。治疗组口服阿托伐他汀钙片1片/次,1次/d,坎地沙坦酯片的用法用量同对照组。两组患者均连续治疗10周。观察两组的临床疗效,同时比较治疗前后两组患者收缩压、舒张压、超敏C反应蛋白(hs-CPR)、内皮素(ET)、一氧化氮(NO)的变化。结果治疗后,两组总有效率分别为76.67%、90.67%,两组比较差异有统计学意义(P0.05)。治疗后,两组患者收缩压、舒张压、hs-CRP、ET均较治疗前显著降低,NO显著升高,同组治疗前后比较差异有统计学意义(P0.05);且治疗组这些观察指标的改善程度优于对照组,两组比较差异有统计学意义(P0.05)。结论阿托伐他汀联合坎地沙坦酯治疗原发性高血压具有较好的临床疗效,可改善患者的血管内皮功能和炎症反应,值得在临床上进一步推广和应用。 相似文献