Hood V L, Dunn M J
Prostaglandins. 1978 Feb;15(2):273-80. doi: 10.1016/0090-6980(78)90166-1.
Potassium-deficiency was induced in rats by dietary deprivation of potassium. The animals became polyuric and urine osmolality decreased more then three-fold compared to controls. Urinary excretion of prostaglandin E2 (PGE2) and prostaglandin F2alpha (PGF2alpha) did not increase during 2 weeks of potassium depletion. Partial inhibition of renal prostaglandin synthesis by meclofenamate did not increase the urine osmolality after water deprivation. These results make unlikely the hypothesis that the polyuria of potassium-deficiency, is the result of enhanced renal synthesis of prostaglandins with subsequent antagonism of the hydro-osmotic effect of vasopressin. Male animals consistently excreted less PGE2 than female animals.
通过饮食中缺钾诱导大鼠出现钾缺乏。与对照组相比,这些动物出现多尿,尿渗透压降低了三倍多。在缺钾的两周内,前列腺素E2(PGE2)和前列腺素F2α(PGF2α)的尿排泄量没有增加。甲氯芬那酸对肾前列腺素合成的部分抑制在禁水后并未增加尿渗透压。这些结果使得缺钾性多尿是由于肾前列腺素合成增强并随后拮抗血管加压素的水渗透作用这一假说不太可能成立。雄性动物排泄的PGE2始终少于雌性动物。