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急性β受体阻滞剂治疗后原发性高血压患者动态运动期间β肾上腺素能受体-cAMP系统的调节

Regulation of the beta-adrenoceptor-cAMP-system during dynamic exercise in patients with primary hypertension after acute beta-blockade.

作者信息

Middeke M, Reder S, Holzgreve H

机构信息

Medizinische Poliklink, Klinikum Innenstadt, Lugwig-Maximilians-Universität, München, Germany.

出版信息

Blood Press. 1994 May;3(3):189-92. doi: 10.3109/08037059409102251.

DOI:10.3109/08037059409102251
PMID:7915172
Abstract

Beta-adrenoceptors on lymphocytes are acutely increased after dynamic exercise in normotensive subjects, but not in hypertensives. It was thus of interest to evaluate the acute regulation of the lymphocyte beta-adrenoceptor-adenylate-cyclase-cAMP-system (BAAS) in patients with primary hypertension during dynamic stress after acute beta-blockade. Density and affinity of beta 2-adrenoceptors, and intracellular cAMP concentrations (baseline and isoprenaline stimulated values) were measured on the peripheral mononuclear cells in 8 male patients with primary hypertension before and immediately after dynamic exercise on a bicycle (50-200 W) at baseline and after acute beta-blockade (2 h following 100 mg atenolol). Dynamic exercise causes no significant changes in receptor density and affinity, nor in basal cAMP values. After acute beta-blockade the dynamic stress-induced rise in mean arterial blood pressure was significantly (p < 0.01) reduced from 33 to 24 mmHg, and beta-adrenoceptor density significantly (p < 0.05) increased from 1320 to 2102 molecules/cell, whereas affinity remained unchanged. Baseline and stimulated cAMP concentrations increased significantly (p < 0.05) from 5.3 to 7.0 and from 2.1 to 3.5 pmol/10(6) cells, respectively. These findings suggest that in primary hypertension the regulation of the beta 2-adrenoceptor-adenylate-cyclase-cAMP-system is impaired on exercise and can be normalised by acute beta-blockade. Since atenolol predominantly blocks beta 1-adrenoceptors, the observed normalisation of the lymphocyte BAAS may reflect only an unspecific effect of antihypertensive therapy per se.

摘要

血压正常的受试者在进行动态运动后,淋巴细胞上的β-肾上腺素能受体急剧增加,但高血压患者则不然。因此,评估急性β受体阻滞剂治疗后,原发性高血压患者在动态应激期间淋巴细胞β-肾上腺素能受体-腺苷酸环化酶-cAMP系统(BAAS)的急性调节情况具有重要意义。在8名男性原发性高血压患者中,于基线状态以及急性β受体阻滞剂治疗后(服用100 mg阿替洛尔2小时后),在自行车上进行动态运动(50 - 200 W)之前及之后,测量外周血单个核细胞上β2-肾上腺素能受体的密度和亲和力,以及细胞内cAMP浓度(基线值和异丙肾上腺素刺激值)。动态运动对受体密度、亲和力以及基础cAMP值均无显著影响。急性β受体阻滞剂治疗后,动态应激引起的平均动脉血压升高显著(p < 0.01)降低,从33 mmHg降至24 mmHg,β-肾上腺素能受体密度显著(p < 0.05)增加,从1320个分子/细胞增至2102个分子/细胞,而亲和力保持不变。基线和刺激后的cAMP浓度分别显著(p < 0.05)升高,从5.3 pmol/10⁶细胞增至7.0 pmol/10⁶细胞,以及从2.1 pmol/10⁶细胞增至3.5 pmol/10⁶细胞。这些发现表明,在原发性高血压患者中,运动时β2-肾上腺素能受体-腺苷酸环化酶-cAMP系统的调节受损,急性β受体阻滞剂治疗可使其恢复正常。由于阿替洛尔主要阻断β1-肾上腺素能受体,观察到的淋巴细胞BAAS恢复正常可能仅反映了抗高血压治疗本身的非特异性作用。

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