Tahira H
Nihon Naibunpi Gakkai Zasshi. 1976 Feb 20;52(2):125-37. doi: 10.1507/endocrine1927.52.2_125.
The renin-angiotensin system, potassium and adrenocorticotropin (ACTH) are well known as control mechanism for aldosterone secretion. However, the precise mechanism of these factors for aldosterone secretion remain still unclear. Several interesting evidences related to the effects of Coenzyme Q on the secretion and biosynthesis of aldosterone have been demonstrated. Biochemical action of Coenzyme Q is generally accepted as a component of the electron transfer process of respiration in mitochondria. Fabre et al demonstrated that significant reduction of plasma aldosterone concentration in adrenal venous by the Coenzyme Q infusion. Weinstein et al observed that urine sodium excretion decreased after infusion of Coenzyme Q into renal artery. Kumagai et al suggested that Coenzyme Q inhibited the activity of 18-hydroxylase in the adrenal cortex. The present study was designed to evaluate the effects of Coenzyme Q on the secretion of aldosterone.
24 cases of male among el and beagle dogs were subdivided into 4 groups. 1st group were administered intravenous infusion of Coenzyme Q, 2nd group were orally administered Coenzyme Q for 7 weeks, 3rd group were administered simultaneous infusion of Coenzyme Q and angiotensin II and 4th group were administered furosemide orally under the condition of continuous Coenzyme Q administration. Then, plasma concentrations of aldosterone, 11-OHCS and angiotensin I were determined during the time course.
Plasma aldosterone concentration was significantly increased after intravenous infusion of angiotensin II and decreased 45 minutes after the beginning of infusion. However, the concentration still remained higher than control level. By the simultaneous infusion of Coenzyme Q with angiotensin II, the decreased concentration again increased significantly. It seems that above mentioned results suggest possibility that Coenzyme Q potentiate the action of angiotensin II on aldosterone secretion. By the intravenous infusion of Coenzyme Q, plasma aldosterone concentration increased significantly and concentrations of plasma 11-OHCS and angiotensin I did not affected. This result suggests that Coenzyme Q may stimulate aldosterone secretion from adrenal cortex without increase of ACTH and renin-angiotensin. 4 hours after the oral administration of Coenzyme Q, plasma aldosterone concentration was increased significantly. Na/K in 24 hours' excreta was decreased by Coenzyme Q administration. The decrease of Na/K in excreta may be reflection of the increase of aldosterone secretion. Although, plasma aldosterone concentration increased for the short duration by the Coenzyme Q, it decreased gradually and returned to the control level after 7 days under the condition of continuous oral administration. By the oral administration of furosemide under prolonged Coenzyme Q administration plasma aldosterone concentration increased significantly and remained higher than that of control.
肾素-血管紧张素系统、钾和促肾上腺皮质激素（ACTH）是众所周知的醛固酮分泌控制机制。然而，这些因素影响醛固酮分泌的精确机制仍不清楚。已经证实了一些与辅酶Q对醛固酮分泌和生物合成的影响相关的有趣证据。辅酶Q的生化作用通常被认为是线粒体呼吸电子传递过程的一个组成部分。法布等人证明，通过输注辅酶Q可使肾上腺静脉血浆醛固酮浓度显著降低。温斯坦等人观察到，向肾动脉输注辅酶Q后尿钠排泄减少。熊谷等人认为辅酶Q抑制肾上腺皮质中18-羟化酶的活性。本研究旨在评估辅酶Q对醛固酮分泌的影响。
将24只雄性埃尔犬和比格犬分为4组。第1组静脉输注辅酶Q，第2组口服辅酶Q 7周，第3组同时输注辅酶Q和血管紧张素II，第4组在持续给予辅酶Q的条件下口服速尿。然后，在整个过程中测定血浆醛固酮、11-羟皮质类固醇和血管紧张素I的浓度。
静脉输注血管紧张素II后血浆醛固酮浓度显著升高，并在输注开始后45分钟下降。然而，该浓度仍高于对照水平。通过将辅酶Q与血管紧张素II同时输注，下降的浓度再次显著升高。上述结果似乎表明辅酶Q增强血管紧张素II对醛固酮分泌作用的可能性。通过静脉输注辅酶Q，血浆醛固酮浓度显著升高，而血浆11-羟皮质类固醇和血管紧张素I的浓度不受影响。这一结果表明辅酶Q可能刺激肾上腺皮质分泌醛固酮，而不增加ACTH和肾素-血管紧张素。口服辅酶Q 4小时后，血浆醛固酮浓度显著升高。给予辅酶Q后24小时排泄物中的钠/钾降低。排泄物中钠/钾的降低可能反映了醛固酮分泌的增加。虽然，辅酶Q使血浆醛固酮浓度在短时间内升高，但在持续口服给药的条件下，7天后逐渐下降并恢复到对照水平。在长期给予辅酶Q的情况下口服速尿，血浆醛固酮浓度显著升高并保持高于对照水平。
