Zacharieva S, Koev D, Matrozov P, Tcharaktchiev D, Stoeva I, Andonova K
Institute of Endocrinology and Gerontology, Medical Academy, Sofia.
Acta Physiol Pharmacol Bulg. 1989;15(4):31-6.
Seven healthy male volunteers were studied at the end of 7 days placebo period and after 7 days treatment with verapamil (120 mg twice daily). Verapamil increased significantly plasma renin activity and urinary excretion of 6-keto prostaglandin F1 alpha without significant modification of plasma aldosterone. Metoclopramide (10 mg i. v.) induced a significant increase of plasma aldosterone with the peak values 15 min after the injection of the drug. The results indicate that verapamil does not lead to secondary hyperaldosteronism which is characteristic of most other vasodilators. The increase of prostacyclin, measured as 6-keto prostaglandin F1 alpha can contribute to the efficacy of verapamil in patients with ischemic heart disease and hypertension. The present study suggests that the aldosterone response to metoclopramide is not directly dependent on calcium, but an indirect effect of calcium through renin-angiotensin system cannot be excluded.
在7天安慰剂期结束时以及用维拉帕米(每日两次,每次120毫克)治疗7天后,对7名健康男性志愿者进行了研究。维拉帕米显著增加了血浆肾素活性和6-酮-前列腺素F1α的尿排泄量,而血浆醛固酮没有显著改变。甲氧氯普胺(静脉注射10毫克)可使血浆醛固酮显著增加,在注射药物后15分钟达到峰值。结果表明,维拉帕米不会导致大多数其他血管扩张剂所特有的继发性醛固酮增多症。以6-酮-前列腺素F1α衡量的前列环素增加可能有助于维拉帕米对缺血性心脏病和高血压患者的疗效。本研究表明,醛固酮对甲氧氯普胺的反应并非直接依赖于钙,但不能排除钙通过肾素-血管紧张素系统产生的间接作用。