TY - JOUR
T1 - Changes in prostacyclin and thromboxane biosynthesis and their catabolic enzyme activity in kidneys of aging rats
AU - Chang, Wen Chang
AU - Tai, Hsin Hsiung
N1 - Funding Information:
The authors wish to thank the National Institute on Aging, NIH for the supply of animals and to Mrs. Sharon Parker for her excellent technical assistance. Thanks are also due to Mr. Rong-Fong Shen for his assistance in the preparation of prostaglandin H2, and to The Upjohn Co., Kalamazoo, MI, U.S.A. and Ono Pharmaceutical Co., Osaka, Japan for the supply of prostaglandin and thromboxane B 2 standards. We are indebted to MrSw~s. West for her assistance in the preparation of the manuscript. This work supported in part from the American Heart Association Kentucky Affiliate, Inc., the University of Kentucky Isabell L. Kircher Fund, the National Institutes of Health (GM 30380) and the American Heart Association (81-1152).
PY - 1984/3/26
Y1 - 1984/3/26
N2 - The effects of aging on the prostacyclin and thromboxane biosynthesis and prostaglandin catabolic enzyme activity in rat kidney were investigated. The prostacyclin biosynthesis, using arachidonic acid as substrate, was the greatest in young kidneys (2 months old) and then progressively decreased in mature (12 months old) and old (24 months old) kidneys, while thromboxane biosynthetic activity showed no significant change as a function of age. When prostaglandin H2 was used as substrate, the prostacyclin and thromboxane biosynthesis showed similar results as when arachidonic acid was used as substrate; the prostacyclin biosynthesis progressively decreased and thromboxane biosynthesis showed no significant change as a function of age. The fatty acid cyclooxygenase in kidney was measured by a specific radioimmunoassay. No significant change in renal fatty acid cyclooxygenase as a function of age was found. Thus, we concluded that the progressive decrease in renal prostacyclin biosynthesis as a function of age is due to a defect in prostacyclin synthetase in aged kidneys. The prostaglandin catabolic enzyme, NAD+-dependent 15-hydroxyprostaglandin dehydrogenase, in kidneys was also investigated. The enzyme activity progressively decreased as a function of age, which suggested a decrease in the metabolism of thromboxane A2 in aged kidneys. The present results, indicating a decrease in renal prostacyclin biosynthesis and renal 15-hydroxyprostaglandin dehydrogenase activity with aging, might contribute to a plausible explanation of the progressive decrease in renal functions in the elderly.
AB - The effects of aging on the prostacyclin and thromboxane biosynthesis and prostaglandin catabolic enzyme activity in rat kidney were investigated. The prostacyclin biosynthesis, using arachidonic acid as substrate, was the greatest in young kidneys (2 months old) and then progressively decreased in mature (12 months old) and old (24 months old) kidneys, while thromboxane biosynthetic activity showed no significant change as a function of age. When prostaglandin H2 was used as substrate, the prostacyclin and thromboxane biosynthesis showed similar results as when arachidonic acid was used as substrate; the prostacyclin biosynthesis progressively decreased and thromboxane biosynthesis showed no significant change as a function of age. The fatty acid cyclooxygenase in kidney was measured by a specific radioimmunoassay. No significant change in renal fatty acid cyclooxygenase as a function of age was found. Thus, we concluded that the progressive decrease in renal prostacyclin biosynthesis as a function of age is due to a defect in prostacyclin synthetase in aged kidneys. The prostaglandin catabolic enzyme, NAD+-dependent 15-hydroxyprostaglandin dehydrogenase, in kidneys was also investigated. The enzyme activity progressively decreased as a function of age, which suggested a decrease in the metabolism of thromboxane A2 in aged kidneys. The present results, indicating a decrease in renal prostacyclin biosynthesis and renal 15-hydroxyprostaglandin dehydrogenase activity with aging, might contribute to a plausible explanation of the progressive decrease in renal functions in the elderly.
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U2 - 10.1016/0024-3205(84)90550-2
DO - 10.1016/0024-3205(84)90550-2
M3 - Article
C2 - 6423922
AN - SCOPUS:0021324950
VL - 34
SP - 1269
EP - 1280
JO - Life Sciences
JF - Life Sciences
SN - 0024-3205
IS - 13
ER -