Marsh A C, Gibson K J, Wu J, Owens P C, Owens J A, Lumbers E R
School of Physiology and Pharmacology, University of New South Wales, Sydney, NSW 2052, Australia.
J Physiol. 2001 Jan 15;530(Pt 2):253-62. doi: 10.1111/j.1469-7793.2001.0253l.x.
While it is known that treatment with insulin-like growth factor I (IGF-I) stimulates growth of the fetal kidney, nothing is known about the short term or long term effects of IGF-I on fetal renal function. To investigate the acute effects of IGF-I on fetal renal function and on the activity of the fetal renin-angiotensin system, studies were carried out in 12 chronically catheterized fetal sheep aged 120 +/- 1 days, before and during a 4 h I.V. infusion of IGF-I at 80 ug h-1. Seven control fetuses were infused over the same period with vehicle (0.1% bovine serum albumin in 0.15 M saline). IGF-I infusion increased plasma IGF-I concentrations by about 80%. There was a small fall in arterial PO2 (P < 0.01), arterial PCO2 increased (P < 0.05), plasma lactate levels increased (P < 0.01) and arterial pH fell (P < 0.05). Fractional bicarbonate reabsorption increased and bicarbonate excretion decreased (P < 0.05). Infusions of IGF-I had no sustained effect on fetal arterial pressure. Glomerular filtration rate (GFR) did not change significantly during IGF-I infusion, but renal blood flow (RBF) fell (P < 0.05). Therefore filtration fraction relative to control values increased (P < 0.05), suggesting that efferent arteriolar vasoconstriction had occurred. IGF-I infusion led to an antidiuresis (P < 0.01), a rise in urinary osmolality (P < 0.05) and a fall in free water clearance (P < 0.01). Since fetal PO2 fell, it is probable that these effects were mediated by arginine vasopressin. The excretion rates of sodium, chloride and phosphate were all reduced by 4 h of infusion (P < 0.05), because their fractional reabsorption rates were all increased (sodium, P < 0.01; chloride, P < 0.01; and phosphate, P < 0.05). Plasma renin concentration increased by 275 +/- 52% during infusion of IGF-I (P < 0.005). Plasma renin activity also increased (P < 0.005), while circulating angiotensinogen concentrations fell (P < 0.05). In the adult, IGF-I increases both RBF and GFR, enhances tubular reabsorption and stimulates the renin-angiotensin system. In the fetus, however, it decreased RBF and had no effect on GFR, but was associated with enhanced tubular function and intense stimulation of renin secretion. Some of these effects of IGF-I on fetal renal function may be involved in maturation of the kidney in preparation for life after birth.
虽然已知用胰岛素样生长因子I(IGF-I)治疗可刺激胎儿肾脏生长,但关于IGF-I对胎儿肾功能的短期或长期影响却一无所知。为了研究IGF-I对胎儿肾功能和胎儿肾素-血管紧张素系统活性的急性影响,对12只年龄为120±1天、长期插管的胎儿绵羊进行了研究,在静脉输注80μg/h的IGF-I之前和输注4小时期间进行观察。7只对照胎儿在同一时期输注赋形剂(0.15M盐水中的0.1%牛血清白蛋白)。输注IGF-I使血浆IGF-I浓度增加约80%。动脉血氧分压略有下降(P<0.01),动脉血二氧化碳分压升高(P<0.05),血浆乳酸水平升高(P<0.01),动脉血pH值下降(P<0.05)。碳酸氢盐重吸收分数增加,碳酸氢盐排泄减少(P<0.05)。输注IGF-I对胎儿动脉压没有持续影响。在输注IGF-I期间,肾小球滤过率(GFR)没有显著变化,但肾血流量(RBF)下降(P<0.05)。因此,相对于对照值,滤过分数增加(P<0.05),提示发生了出球小动脉血管收缩。输注IGF-I导致抗利尿(P<0.01),尿渗透压升高(P<0.05),自由水清除率下降(P<0.01)。由于胎儿血氧分压下降,这些影响可能是由精氨酸加压素介导的。输注4小时后,钠、氯和磷酸盐的排泄率均降低(P<0.05),因为它们的重吸收分数均增加(钠,P<0.01;氯,P<0.01;磷酸盐,P<0.05)。在输注IGF-I期间,血浆肾素浓度增加了275±52%(P<0.005)。血浆肾素活性也增加(P<0.005),而循环血管紧张素原浓度下降(P<0.05)。在成年人中,IGF-I可增加肾血流量和肾小球滤过率,增强肾小管重吸收并刺激肾素-血管紧张素系统。然而,在胎儿中,它降低了肾血流量,对肾小球滤过率没有影响,但与肾小管功能增强和肾素分泌的强烈刺激有关。IGF-I对胎儿肾功能的这些影响中的一些可能参与了肾脏的成熟,为出生后的生活做准备。