Circulating coupling factor 6 in human hypertension: role of reactive oxygen species.
OBJECTIVE
Coupling factor 6 is an endogenous inhibitor of prostacyclin synthesis and might function as an endogenous vasoconstrictor in the fashion of a circulating hormone in rats. We investigated the role of coupling factor 6 in human hypertension.


RESULTS
The patients with essential hypertension (EH) (n = 30) received a series of normal salt diet (12 g salt/day) for 3 days, low salt diet (2 g salt/day) for 7 days, and high salt diet (20-23 g salt/day) for 7 days. Normotensive control subjects (n = 27) received normal and low salt diets. The plasma level of coupling factor 6, measured by radioimmunoassay, during normal salt diet was higher in patients with EH than in normotensive subjects (17.6 +/- 1.7 versus 12.8 +/- 0.5 ng/ml, P < 0.01). Whereas the plasma level of coupling factor 6 was unchanged after salt restriction in normotensive subjects, it was decreased after salt restriction (from 12 g/day to 2 g/day) and was increased after salt loading (from 2 g/day to 20-23 g/day) in patients with EH. This increase in plasma level of coupling factor 6 was abolished by oral administration of ascorbic acid, but the level of blood pressure was unaffected. The percentage changes in plasma coupling factor 6 level after salt restriction and loading were positively correlated with those in mean blood pressure (r = 0.57, P < 0.01), and negatively correlated with those in plasma nitric oxide level (r = -0.51, P < 0.05).


CONCLUSIONS
These indicate that circulating coupling factor 6 is elevated in human hypertension and modulated by salt intake presumably via reactive oxygen species.
Osanai
Tomohiro
T
Second Deparment of Internal Medicine, Hirosaki University School of Medicine, Japan. osanait@cc.hirosaki-u.ac.jp
Sasaki
Satoko
S
Kamada
Takaatsu
T
Fujiwara
Naoto
N
Nakano
Takao
T
Tomita
Hirofumi
H
Matsunaga
Toshiro
T
Magota
Koji
K
Okumura
Ken
K
D000975:Antioxidants / Q000008:administration & dosage; D001205:Ascorbic Acid / Q000008:administration & dosage; D015415:Biomarkers / Q000097:blood; D001794:Blood Pressure / Q000187:drug effects; D004039:Diet, Sodium-Restricted; D015237:Dinoprost / Q000031:analogs & derivatives / Q000097:blood; D042783:Endothelial Cells / Q000187:drug effects / Q000378:metabolism; D005260:Female; D006801:Humans; D006973:Hypertension / Q000097:blood* / Q000503:physiopathology; D008297:Male; D008875:Middle Aged; D025261:Mitochondrial Proton-Translocating ATPases / Q000097:blood* / Q000187:drug effects; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D010086:Oxidative Phosphorylation Coupling Factors / Q000097:blood* / Q000187:drug effects; D017382:Reactive Oxygen Species / Q000378:metabolism; D012083:Renin / Q000378:metabolism; D012982:Sodium, Dietary / Q000008:administration & dosage; D013223:Statistics as Topic
D000975:Antioxidants; D015415:Biomarkers; D009566:Nitrates; D009573:Nitrites; D010086:Oxidative Phosphorylation Coupling Factors; D017382:Reactive Oxygen Species; D012982:Sodium, Dietary; C075750:8-epi-prostaglandin F2alpha; D015237:Dinoprost; D012083:Renin; C000628217:F(6) ATPase; D025261:Mitochondrial Proton-Translocating ATPases; D001205:Ascorbic Acid; D009638:Norepinephrine