Rathaus M, Magen A, Rath-Wolfson L, Shapira J, Bernheim J
Isr J Med Sci. 1983 Dec;19(12):1072-4.
The urinary excretion of prostaglandins (PG) E2 and F2 alpha was measured by radioimmunoassay in 15 patients with essential hypertension, before and after 2 and 4 weeks of treatment with the selective beta 1-adrenergic blocker, atenolol. Systolic and diastolic blood pressure, pulse rate and plasma renin activity decreased significantly during the treatment. No change was observed in renal function and electrolyte balance. The 24-hour excretion of PGE2 and PGF2 alpha was also unaffected by the antihypertensive treatment. The above findings, in contrast with those previously observed with another beta-blocker, propranolol, suggest that tubular beta-receptors are not involved in the synthesis of PGs. The different hemodynamic effects of the two drugs are the most likely explanation for the different responses in prostaglandin excretion.
采用放射免疫分析法测定了15例原发性高血压患者在使用选择性β1 - 肾上腺素能阻滞剂阿替洛尔治疗2周和4周前后前列腺素(PG)E2和F2α的尿排泄量。治疗期间收缩压和舒张压、脉率及血浆肾素活性显著下降。肾功能和电解质平衡未见变化。抗高血压治疗对PGE2和PGF2α的24小时排泄量也无影响。上述发现与先前使用另一种β受体阻滞剂普萘洛尔时观察到的结果相反,提示肾小管β受体不参与PG的合成。两种药物不同的血流动力学效应最有可能解释前列腺素排泄的不同反应。