Effect of potassium supplementation on blood pressure and vasodilator mechanisms in spontaneously hypertensive rats.
Effect of potassium supplementation on blood pressure and vasodilator mechanisms in spontaneously hypertensive rats.
复制标题
补充钾对自发性高血压大鼠血压和血管舒张机制的影响。
作者：
Anne Barden;Lawrence J. Beilin;R. Vandongen
1.补充1%（w/v）KCl溶液显著减弱了自发性高血压大鼠中通常观察到的血压随年龄的升高，导致5周后血压差异为18 mmHg。2.在接受钾的大鼠中，尿6-酮-前列腺素F1 α（前列环素的稳定水解产物）和激肽释放酶排泄显著升高。3.在补钾的最初几天内，未观察到钠排泄量差异;然而，补钾动物在5周内排泄的钠相对较多。4. 5周后，接受钾的动物血浆肾素活性显著降低。5.有人提出，增加全身和/或肾脏前列环素和激肽释放酶合成的组合，结合降低肾素活性，有助于钾补充自发性高血压大鼠的血压衰减。
1. Supplementation with 1% (w/v) KCl solution significantly attenuated the blood pressure rise with age normally observed in spontaneously hypertensive rats, resulting in a difference in blood pressure of 18 mmHg after 5 weeks. 2. Urinary 6-keto-prostaglandin F1 alpha (the stable hydrolysis product of prostacyclin) and kallikrein excretion were significantly elevated in rats receiving potassium. 3. No difference was observed in sodium excretion during the initial days of potassium supplementation; however, the potassium-supplemented animals excreted relatively more sodium over the 5 week period. 4. Plasma renin activity was significantly reduced in those animals receiving potassium after 5 weeks. 5. It is proposed that a combination of increased systemic and/or renal prostacyclin and kallikrein synthesis may, in combination with reduced renin activity, contribute to the attenuation of blood pressure in potassium-supplemented spontaneously hypertensive rats.