Cyclosporine augments renal mitochondrial function in vivo and reduces renal blood flow.
The in vivo action of cyclosporine A (CS) on rat renal cortical mitochondria was investigated. CS (30 mg.kg-1.day-1) given orally to rats for 30 days caused an augmentation of renal mitochondrial oxidative phosphorylation. The ADP-stimulated respiratory rate was increased by 37.0% with glutamate plus malate as respiratory substrates (P less than 0.025) but not with succinate-supported respiration, indicating enhancement of mitochondrial complex I activity. This reaction may be a response to the 32.5% reduction of renal blood (P less than 0.005) in the CS-treated group, possibly serving to maximize ATP synthesis during ischemia. Ligation-induced decreases in renal blood flow also resulted in enhancement of mitochondrial complex I activity.
Lemmi
C A
CA
Department of Anatomy and Cell Biology, University of California, Los Angeles 90024.
Pelikan
P C
PC
Sikka
S C
SC
Hirschberg
R
R
Geesaman
B
B
Miller
R L
RL
Park
K S
KS
Liu
S C
SC
Koyle
M
M
Rajfer
J
J
D000818:Animals; D003524:Cyclosporins / Q000494:pharmacology*; D000860:Hypoxia / Q000503:physiopathology; D007668:Kidney / Q000187:drug effects / Q000502:physiology* / Q000648:ultrastructure; D007672:Kidney Cortex / Q000502:physiology / Q000648:ultrastructure; D007674:Kidney Diseases / Q000503:physiopathology; D008026:Ligation; D008297:Male; D008928:Mitochondria / Q000187:drug effects / Q000502:physiology*; D010101:Oxygen Consumption / Q000187:drug effects; D051381:Rats; D011919:Rats, Inbred Strains; D012079:Renal Circulation / Q000187:drug effects*
D003524:Cyclosporins