Linas S L, Dickmann D
Kidney Int. 1982 May;21(5):757-64. doi: 10.1038/ki.1982.94.
Although chronic potassium deficiency is a common clinical problem, the hemodynamic consequences of chronic sustained potassium depletion have not been clearly delineated. In this study, the hemodynamic consequences of chronic potassium depletion were evaluated in the conscious rat. Potassium-depleted rats had a decrease in mean arterial pressure which was caused by a decrease in systemic vascular resistance. In association with these changes in systemic hemodynamics, renal blood flow (RBF) was also decreased. The decreased renal blood flow was caused by an increased renal vascular resistance (RVR). Because plasma renin activity was increased the role of angiotensin II as a renal vasoconstrictor was evaluated by utilizing two angiotensin antagonists. Although the administration of saralasin to potassium-depleted rats did not alter systemic hemodynamics, RVR was decreased and RBF was increased. Similar results were obtained with the converting enzyme inhibitor teprotide. Because products of endoperoxide metabolism may cause renal vasoconstriction, the role of prostaglandins and thromboxanes as renal vasoconstrictors were evaluated by utilizing cyclo-oxygenase and thromboxane synthetase inhibitors. None of these agents altered systemic hemodynamics. Following the administration of indomethacin, RVR was decreased and RBF was increased in potassium-depleted rats. Similar results were obtained with another cyclo-oxygenase inhibitor, meclofenamate, and with imidazole, an inhibitor of thromboxane synthetase. Because neither angiotensin II nor products of endoperoxide metabolism could alone account for the increased renal vascular resistance of potassium depletion, studies were performed in potassium-depleted rats treated with indomethacin plus either saralasin or teprotide. In these potassium-depleted animals, renal blood flow was restored to normal. In conclusion, the decrease in renal blood flow and the increase in renal vascular resistance in potassium depletion is mediated by angiotensin II and a product of prostaglandin endoperoxide metabolism, most likely, thromboxane.
尽管慢性钾缺乏是一个常见的临床问题，但慢性持续性钾耗竭对血流动力学的影响尚未明确界定。在本研究中，对清醒大鼠慢性钾耗竭的血流动力学影响进行了评估。钾缺乏的大鼠平均动脉压降低，这是由全身血管阻力降低所致。与这些全身血流动力学变化相关的是，肾血流量（RBF）也降低。肾血流量降低是由肾血管阻力（RVR）增加引起的。由于血浆肾素活性增加，利用两种血管紧张素拮抗剂评估了血管紧张素II作为肾血管收缩剂的作用。尽管给钾缺乏的大鼠注射沙拉新并未改变全身血流动力学，但肾血管阻力降低，肾血流量增加。使用转化酶抑制剂替普罗肽也得到了类似的结果。由于内过氧化物代谢产物可能导致肾血管收缩，利用环氧化酶和血栓素合成酶抑制剂评估了前列腺素和血栓素作为肾血管收缩剂的作用。这些药物均未改变全身血流动力学。给钾缺乏的大鼠注射吲哚美辛后，肾血管阻力降低，肾血流量增加。使用另一种环氧化酶抑制剂甲氯芬那酸以及血栓素合成酶抑制剂咪唑也得到了类似的结果。由于血管紧张素II和内过氧化物代谢产物均不能单独解释钾缺乏时肾血管阻力的增加，因此对用吲哚美辛加沙拉新或替普罗肽治疗的钾缺乏大鼠进行了研究。在这些钾缺乏的动物中，肾血流量恢复正常。总之，钾缺乏时肾血流量的减少和肾血管阻力的增加是由血管紧张素II和前列腺素内过氧化物代谢产物（很可能是血栓素）介导的。
