Effect of nicotine on the formation of prostaglandins in the rabbit kidney

Summary. The effect of nicotine on the conversion of 14 C‐labelled arachidonate ( 14 C‐AA) to 14 C‐labelled primary prostaglandins (PGs) was investigated in low‐speed super‐natants and high‐speed sediments of rabbit homogenized kidneys. Nicotine (2×10˜ 7 M‐2×10 _4 M) dose‐dependently inhibited the formation of the labelled PGs D 2 , E 2 and F 2a regardless of whether low‐speed supernatants or high‐speed sediments were the enzymatic source. The (I). 0 of nicotine was about 10 ‐5 M. Nicotine did not affect the distribution of the primary PGs formed in comparison to controls. Indomethacin also inhibited the formation of labelled PGs, being on a molar basis about 500 times more efficient than nicotine. It is concluded that nicotine attenuates the bioformation of primary PGs in the rabbit kidney, probably by eliciting an inhibitory effect on the cyclo‐oxygenase that converts A A to PGendoperoxides.