Machida J, Ueda S, Yoshida M, Soejima H, Ikegami K
Department of Urology, Kumamoto University Medical School, Japan.
Nephron. 1988;49(1):74-80. doi: 10.1159/000184990.
To study the role of sodium and renal prostaglandin E2 in the chronic phase of two-kidney one-clip renovascular hypertension, urinary excretion rates of sodium and prostaglandin E2 were measured in rabbits with hypertension induced by left renal artery constriction during alteration in sodium intake. The arterial blood pressure, the increasing rate of body weight and sodium balance during alteration in sodium intake were directly proportional to the amount of sodium intake in the hypertensive rabbits, but not in the control ones. Plasma renin activity and plasma aldosterone concentration, which had no significant difference between hypertensive and control rabbits, were inversely proportional to the amount of sodium intake in both rabbits. Urinary excretion rates of sodium in the clipped kidneys of the hypertensive rabbits were significantly lower than the control values in all dietary regimens (p less than 0.01). Urinary excretion rates of sodium in the nonclipped kidneys were not significantly higher and in the total kidneys were significantly lower than the corresponding control values during sodium load (p less than 0.01). Urinary excretion rates of prostaglandin E2 were inversely proportional to the amount of sodium intake in both groups. Urinary excretion rates of prostaglandin E2 in the clipped kidneys were significantly lower than the control values in all dietary regimens (p less than 0.001). Urinary excretion rates of prostaglandin E2 in the nonclipped kidneys were significantly higher during sodium restriction (p less than 0.01) but not during sodium load than the control values. Furthermore, urinary excretion rates of prostaglandin E2 in the total kidneys were significantly lower than the control values in all dietary regimens (p less than 0.01). These results suggest that two-kidney one-clip renovascular hypertension in rabbits seems to be partly sodium-dependent in the chronic phase because the nonclipped kidney fails to excrete sodium sufficiently. There may also be disorders of renal prostaglandin E2 metabolism influencing these disorders of sodium in the nonclipped kidneys.
为研究钠和肾前列腺素E2在两肾一夹肾血管性高血压慢性期的作用，在改变钠摄入量的过程中，对左肾动脉缩窄诱导高血压的家兔，测定其尿钠排泄率和前列腺素E2排泄率。钠摄入量改变期间，高血压家兔的动脉血压、体重增加率和钠平衡与钠摄入量成正比，而对照家兔则不然。高血压家兔与对照家兔的血浆肾素活性和血浆醛固酮浓度无显著差异，二者均与钠摄入量成反比。在所有饮食方案中，高血压家兔夹闭肾的尿钠排泄率均显著低于对照值（p<0.01）。钠负荷期间，未夹闭肾的尿钠排泄率无显著升高，而总肾的尿钠排泄率显著低于相应对照值（p<0.01）。两组中前列腺素E2的尿排泄率均与钠摄入量成反比。在所有饮食方案中，夹闭肾的前列腺素E2尿排泄率均显著低于对照值（p<0.001）。钠限制期间，未夹闭肾的前列腺素E2尿排泄率显著高于对照值（p<0.01），但钠负荷期间则不然。此外，在所有饮食方案中，总肾的前列腺素E2尿排泄率均显著低于对照值（p<0.01）。这些结果表明，家兔两肾一夹肾血管性高血压在慢性期似乎部分依赖于钠，因为未夹闭肾不能充分排泄钠。肾前列腺素E2代谢紊乱可能也影响了未夹闭肾的钠代谢紊乱。
