Reid A F, Coghlan J P, Whitworth J A, Scoggins B A
Howard Florey Institute of Experimental Physiology and Medicine, University of Melbourne, Australia.
Am J Hypertens. 1990 Oct;3(10):775-81. doi: 10.1093/ajh/3.10.775.
This study investigated the ability of two diuretics, amiloride and frusemide, to prevent the development of ACTH induced hypertension in conscious sheep. Infusion of amiloride (20 mg/day) or frusemide (50 mg/day) for three days into normotensive sheep did not have any significant effects on blood pressure. Amiloride blocked ACTH-induced hypertension and the sodium retention and hypokalemia which is usually associated with ACTH administration. Frusemide failed to completely block the hypertension and potassium loss, however it blocked the transient initial urinary sodium retention associated with ACTH-induced hypertension. As frusemide failed to completely block the hypertension it is unlikely that the amiloride effect is due primarily to effects on urinary Na excretion. It is possible that amiloride is exerting its antihypertensive effects by blocking sodium channels.
本研究调查了两种利尿剂（氨氯吡咪和速尿）预防促肾上腺皮质激素（ACTH）诱导的清醒绵羊高血压的能力。向血压正常的绵羊连续三天输注氨氯吡咪（20毫克/天）或速尿（50毫克/天）对血压没有任何显著影响。氨氯吡咪可阻断ACTH诱导的高血压以及通常与ACTH给药相关的钠潴留和低钾血症。然而，速尿未能完全阻断高血压和钾流失，但它阻断了与ACTH诱导的高血压相关的短暂初始尿钠潴留。由于速尿未能完全阻断高血压，氨氯吡咪的作用不太可能主要归因于对尿钠排泄的影响。氨氯吡咪有可能通过阻断钠通道发挥其降压作用。
