Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.
Increased renal secretion of norepinephrine and prostaglandin E2 during sodium depletion in the dog.
复制标题
狗钠消耗期间，去甲肾上腺素和前列腺素 E2 的肾脏分泌增加。
DOI：
10.1172/jci109912
复制
发表时间：
1980
期刊：
影响因子：
--
通讯作者：
Cannon,PJ
中科院分区：
文献类型：
--
作者：
Oliver,JA;Pinto,J;Sciacca,RR;Cannon,PJ
为了确定是否血管活性肾激素调节肾血流量在钠平衡的变化，同时测量动脉和肾静脉浓度的去甲肾上腺素和前列腺素E2（PGE 2）和血浆肾素活性，以及肾血流量和全身血流动力学进行了24钠耗尽和28钠充满麻醉犬。钠耗尽的狗的平均动脉血压与喂食正常钠饮食的动物的平均动脉血压没有显著差异，但心输出量显著较低（3.07 +/- 0.18对3.77 +/- 0.17升/分钟，平均值+/- SEM; P < 0.01）。尽管钠缺乏犬的总外周血管阻力较高（46.1 +/- 2.9 vs. 37.0 +/- 2.1任意阻力U; P < 0.02），但两组的肾血流量和肾血管阻力无显著差异。动脉血浆肾素活性和去甲肾上腺素的浓度在钠耗尽的动物高于对照组;动脉中的PGE 2浓度在两组中相等。肾静脉血浆肾素活性较高，在钠耗尽的狗。同样，钠耗竭犬的肾静脉去甲肾上腺素浓度高于对照犬（457 +/- 44 vs. 196 +/- 25 pg/ml; P < 0.01）;钠耗竭犬的肾静脉PGE 2浓度也高于对照犬（92 +/- 22 vs. 48 +/- 11 pg/ml; P < 0.01）。吲哚美辛给5只钠充足的狗，对肾血流量没有影响。在5只钠缺乏的狗中，吲哚美辛使肾血流量从243 +/- 19降至189 +/- 30 ml/min（P < 0.05），肾静脉血中的PGE 2从71 +/- 14降至15 +/- 2 pg/ml（P < 0.02）。结果表明，中度慢性钠缺乏，除了增强活性的肾素-血管紧张素系统，也增加了肾肾上腺素能神经系统的活性，并增加肾脏PGE 2的合成。在钠耗竭犬中，前列腺素合成的抑制与肾血流量的显著减少相关。结果表明，肾血流量维持在中度钠耗竭的影响，以对抗血管紧张素II和肾交感神经系统的血管收缩作用的洋地黄素。
To determine whether vasoactive renal hormones modulate renal blood flow during alterations of sodium balance, simultaneous measurements of arterial and renal venous concentrations of norepinephrine and prostaglandin E2 (PGE2) and of plasma renin activity, as well as renal blood flow and systemic hemodynamics were carried out in 24 sodium-depleted and 28 sodium-replete anesthetized dogs. The mean arterial blood pressure of the sodium depleted dogs was not significantly different from that of the animals fed a normal sodium diet, but cardiac output was significantly lower (3.07 +/- 0.18 vs. 3.77 +/- 0.17 liters/min, mean +/- SEM; P < 0.01). Despite the higher total peripheral vascular resistance in the sodium-depleted dogs (46.1 +/- 2.9 vs. 37.0 +/- 2.1 arbitrary resistance U; P < 0.02), the renal blood flow and renal vascular resistance were not significantly different in the two groups. The arterial plasma renin activity and concentration of norepinephrine were higher in the sodium-depleted animals than in the controls; the arterial concentration of PGE2 was equal in both groups. The renal venous plasma renin activity was higher in the sodium-depleted dogs. Similarly, the renal venous norepinephrine concentration was higher in the sodium-depleted dogs than in the controls (457 +/- 44 vs. 196 +/- 25 pg/ml; P < 0.01); renal venous PGE2 concentration was also higher in the sodium depleted dogs (92 +/- 22 vs. 48 +/- 11 pg/ml; P < 0.01). Administration of indomethacin to five sodium-replete dogs had no effect on renal blood flow. In five sodium-depleted dogs indomethacin lowered renal blood flow from 243 +/- 19 to 189 +/- 30 ml/min (P < 0.05) and PGE2 in renal venous blood from 71 +/- 14 to 15 +/- 2 pg/ml (P < 0.02). The results indicate that moderate chronic sodium depletion, in addition to enhancing the activity of the renin-angiotensin system, also increases the activity of the renal adrenergic nervous system and increases renal PGE2 synthesis. In sodium-depleted dogs, inhibition of prostaglandin synthesis was associated with a significant decrease in renal blood flow. The results suggest that the renal blood flow is maintained during moderate sodium depletion by an effect of the prostaglandins to oppose the vasoconstrictor effects of angiotensin II and the renal sympathetic nervous system.