Sechi L A, Tedde R, Melis A
Istituto di Clinica Medica Generale, Università di Sassari.
Boll Soc Ital Biol Sper. 1990 Jul;66(7):693-700.
This study has been performed in order to evaluate whether furosemide can induce changes in blood pressure independently of its diuretic effects,and whether its pressor effects are connected with the ability to synthetize renal prostaglandins. The experiments were performed in four groups of volume-expanded rats: the first (n.5) had bilateral ligation of the renal vessels; the second (n.8) had bilateral ligation of the ureters; the third group (n.6) had ureters ligation after pre-treatment with indomethacin; the fourth group (n.2) received a pre-treatment with captopril. After blood pressure stabilization, furosemide was administered i.v. (0.125 mg/100 g. of body weight). Indirect readings of the blood pressure were obtained at 1, 2, 3, 4, 5, 7.5, 10, 15, 20 min. After furosemide administration, blood pressure fell down quickly in the rats with ureteral ligation and in those with captopril pretreatment, while the tensive response to furosemide was blunted by the indomethacin treatment. In conclusion, furosemide can reduce blood pressure by a mechanism non related with its diuretic properties, which, however, requires the integrity of the renal connections with the circulatory system.
本研究旨在评估呋塞米是否能在不依赖其利尿作用的情况下引起血压变化，以及其升压作用是否与合成肾前列腺素的能力有关。实验在四组血容量增加的大鼠中进行：第一组（n = 5）双侧结扎肾血管；第二组（n = 8）双侧结扎输尿管；第三组（n = 6）在吲哚美辛预处理后结扎输尿管；第四组（n = 2）接受卡托普利预处理。血压稳定后，静脉注射呋塞米（0.125 mg/100 g体重）。在给药后1、2、3、4、5、7.5、10、15、20分钟进行间接血压读数。给予呋塞米后，输尿管结扎的大鼠和卡托普利预处理的大鼠血压迅速下降，而吲哚美辛处理使对呋塞米的升压反应减弱。总之，呋塞米可通过与其利尿特性无关的机制降低血压，然而，这需要肾脏与循环系统连接的完整性。
