[Effects of coenzyme Q on plasma aldosterone concentrations in dogs (author's transl)].
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.


METHODS
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.


CONCLUSIONS
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.
D015062:11-Hydroxycorticosteroids / Q000097:blood; D000450:Aldosterone / Q000097:blood*; D000804:Angiotensin II / Q000097:blood; D000818:Animals; D004285:Dogs; D005665:Furosemide / Q000494:pharmacology; D008297:Male; D011188:Potassium / Q000378:metabolism; D012083:Renin / Q000097:blood; D012964:Sodium / Q000378:metabolism; D014451:Ubiquinone / Q000008:administration & dosage / Q000494:pharmacology*
D015062:11-Hydroxycorticosteroids; D000804:Angiotensin II; D014451:Ubiquinone; D000450:Aldosterone; D005665:Furosemide; D012964:Sodium; D012083:Renin; D011188:Potassium