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The review concluded that diuretics and beta-blocker treatments may increase the chances of developing type 2 diabetes.

检讨的结论认为利尿剂和β受体阻滞剂治疗可能增加的机会,发展2型糖尿病。

RESULTS:(1) ET-1 could increase total protein production, surface area, ERKs activity and [Ca2+]i in cultured cardiomyocyte in dose-dependent manner at concentrations ranging from 10-9 to 10-7 mol/L. And this effect could be abolished by BQ123, an antagonist of ETA receptor, partly inhibited by PTX, but not by BQ788, an antagonist of ETB receptor.(2)The activation of ERKs and the increase of [Ca2+]i induced by ET-1 were obviously inhibited by PD98059, a selective ERKs kinase inhibitor, and nifedipine, a calcium channel blocker, respectively. Both antagonists partially inhibited ET-1-stimulated cardiomyocyte hypertrophic response.(3) Staurosporine, a selective PKC inhibitor, could inhibit ET-1-stimulated cardiomyocyte hypertrophic response and increase of [Ca2+]i, but not affect the activation of ERKs.

结果: ①ET-1浓度依赖性增加新生大鼠心肌细胞蛋白质含量和心肌细胞表面积、ERKs活性及[Ca2+]i浓度,以上作用可被ETA受体拮抗剂BQ123所完全抑制,被百日咳毒素部分抑制,而ETB受体拮抗剂BQ788则无效;②ERKs激酶特异性抑制剂PD98059可完全抑制ET-1激活ERKs的作用,钙通道拮抗剂硝苯地平可明显抑制ET-1介导的[Ca2+]i浓度增加,但二者皆仅部分抑制ET-1介导的心肌细胞肥大反应;③蛋白激酶C选择性抑制剂staurosporine并不能明显抑制ET-1介导的ERKs激活,但可抑制ET-1介导的的[Ca2+]i浓度增加及心肌细胞肥大反应。

Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

Methods A total of 34 diabetes patients with hypertension were studied. A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and Ualbumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

A dose of 5 mg imidapril was given daily in treatment group except oral medicine for decreasing glucose level. Ca2+ blocker was given in control group. Their blood glucose level, blood pressure and U??albumin excretions were determined both in the treatment and the control group before and after the treatment.

采用免疫比浊法测定2型糖尿病合并高血压患者的尿微量白蛋白,选择34例尿微量白蛋白正常的患者,随机分为2组,治疗组17人,在口服降糖药的基础上加咪达普利,对照组17人,在口服降糖药的基础上加钙离子拮抗剂,两组治疗前后均监测血压、血糖、糖化血红蛋白和UAE。

I believe it is even superior to those modified forms like nifedipine and GITS which is inherently slow-acting but modified release so not a true long-acting calcium channel blocker which amlodipine is.

而且我认为,氨氯地平优于经过剂型修饰的药物,例如硝苯地平控释片,其本身并不是真正的长效制剂,只是对药物的释放进行了修饰和控制。

Intracerebral ventricular injection of M receptor blocker,Atropine(10 μ L 1× 10- 7 mol/L), failed to block the gastric contraction effect of cerebral SP.

侧脑室注射 M 受体阻断剂阿托品 10 μ L(1× 10- 7 mol/L),不能阻断脑内 P物质对胃的收缩效应。

Pretreatment with KATP channel blocker glibenclamide (Gli; 20μmol/L) could partially block the effects of H2S pretreatment (100μmol/L).

应用KATP通道阻断剂格列苯脲( Gli; 20μmol/L ),可部分阻断H2S对乳头状肌细胞的电生理效应。

In this frame, a pioneer preparation is that containing a low dose of a highly selective b1-blocker (bisoprolol, 2.5 mg) and a low dose of a thiazide diuretic (hydrochlorothiazide, HCTZ, 6.25 mg).

这一领域中的一种开拓性的制剂,含有小剂量的高度选择性b1-阻滞剂(比索洛尔,2.5 mg)和小剂量的噻嗪类利尿剂(氢氯噻嗪,6.25 mg)。

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