REGULATION OF ENDOTHELIN EXCRETION

内皮素(ET)是一种强有力的内源性血管收缩因子，由 内皮素。尿液中ET含量较高，而尿液中ET含量较低 血浆中的水平。尽管人们已经了解了很多关于这个结构的知识 以及ET的生物学效应，但对ET的调节知之甚少。 尿ET排泄量(UETV)。 我们研究了1)血管紧张素II(A-II)、精氨酸的作用 加压素(AVP)和硝苯地平治疗UETV。2)非政府组织的影响 特异性A-II拮抗剂Saralasin和特异性A-II非肽 拮抗剂氯沙坦对A-II对UETV刺激作用的影响3) 卡托普利对转化酶抑制作用的影响 硝苯地平对UETV的影响 A-II(50和500 ng/kg/min)引起尿流量显著增加 (V)、平均动脉压(MAP)和UETV增加10-30倍。 沙拉菌素(1-3 mg)可显著降低大鼠的V 和地图，但不是UETV。仅输注沙拉菌素就能引起显著的 在不影响MAP或V的情况下增加UETV 氯沙坦(10 mg/kg)可完全阻断MAP和MAP的升高 A-II诱导的UETV。AVP(10和100增加/kg/h)给药 引起与A-II类似的高血压和利尿剂反应，但不是 更改UETV。 硝苯地平(0.1和1.0 mg/kg/h)使UETV增加3~10倍。 转化酶抑制剂(卡托普利-卡托普利)对大鼠的影响 1 mg/kg/h)取消了这一增加。

Endothelin (ET), a potent endogenous vasoconstrictor, is produced by the endothelin. High amounts of ET are found in the urine compared to low levels in plasma. Although much has been learned about the structure and biological effects of ET, little is known about the regulation of the urinary excretion of ET (UETV). We investigated 1) The effects of angiotensin II (A-II), arginine vasopressin (AVP) and nifedipine on UETV. 2) The effects of the non specific A-II antagonist - Saralasin and the specific A-II non peptide antagonist - losartan on the stimulatory effect of A-II on UETV. 3) The effect of converting enzyme inhibition by captopril on the stimulatory effect of nifedipine on the UETV. A-II (50 and 500 ng/kg/min) caused significant increases in urine flow (V), mean arterial pressure (MAP) and 10-30 fold increases in UETV. Pretreatment of the rats with saralasin (1-3 mg) significantly reduced V and MAP but not UETV. Infusion of saralasin alone caused a significant increase in UETV without affecting the MAP or V. Pretreatment of the rats with losartan (10 mg/kg) totally blocked the increases in MAP and UETV induced by A-II. AVP (10 and 100 increases/kg/h) administration induced similar hypertensive and diuretic responses as A-II, but did not alter UETV. Infusion of nifedipine (0.1 and 1.0 mg/kg/h) increased UETV 3-10 fold. Pretreatment of the rats with converting enzyme inhibitor (captopril- 1mg/kg/h) abolished that increase.