Steele T H, Challoner-Hue L, Gottstein J H
Miner Electrolyte Metab. 1984;10(1):5-11.
In order to assess the effect of renal prostaglandins on the glomerular filtration rate (GFR) and electrolyte excretion in the spontaneously hypertensive rat (SHR), we perfused isolated SHR and normotensive Wistar-Kyoto (WKY) kidneys after pretreatment with either a control diet or a diet deficient in arachidonate, the precursor of prostaglandins. When perfusion pressures were increased from 100 to 160 mm Hg, renal vascular resistances (RVR) increased by 32-41%. RVR of SHR kidneys always exceeded that of WKY kidneys by a nearly constant amount, and arachidonate deficiency had little effect on this relationship. In contrast to RVR, the GFR increased severalfold. GFR and urine flow were greater in WKY than in SHR kidneys, a relationship unaffected by arachidonate deficiency. Changes in sodium and chloride excretion occurred in parallel with GFR. Although arachidonate-deficient SHR and WKY kidneys manifested potassium wastage compared to controls, arachidonate deficiency did not result in altered sodium or chloride excretion. The results suggest that direct actions of arachidonate or renal prostaglandins are not responsible for most functional differences between SHR and WKY kidneys.
为了评估肾前列腺素对自发性高血压大鼠（SHR）肾小球滤过率（GFR）和电解质排泄的影响，我们在用对照饮食或缺乏前列腺素前体花生四烯酸的饮食预处理后，对分离的SHR和正常血压的Wistar-Kyoto（WKY）大鼠肾脏进行灌注。当灌注压力从100毫米汞柱增加到160毫米汞柱时，肾血管阻力（RVR）增加了32%-41%。SHR肾脏的RVR总是比WKY肾脏的RVR高出几乎恒定的量，花生四烯酸缺乏对这种关系影响不大。与RVR相反，GFR增加了几倍。WKY肾脏的GFR和尿流比SHR肾脏的更大，这种关系不受花生四烯酸缺乏的影响。钠和氯排泄的变化与GFR平行发生。尽管与对照组相比，缺乏花生四烯酸的SHR和WKY肾脏表现出钾流失，但花生四烯酸缺乏并未导致钠或氯排泄的改变。结果表明，花生四烯酸或肾前列腺素的直接作用并非SHR和WKY肾脏之间大多数功能差异的原因。
