Effect of castration on the experimental renal hypertension of the rat. Blood pressure, nephrosclerosis, long-chain fatty acids, and N-acetylation of PAH in the kidney.
Rats were rendered hypertensive by clamping one renal artery. Both kidneys remained in situ ('two-kidney one-clip Goldblatt hypertension'). Half of the animals were simultaneously castrated. 18-24 weeks after the operation both castrated females and males had a lower level of hypertension than the uncastrated controls. The kidneys of castrates contained less connective tissue (measured as the content of hydroxyproline) and long-chain (C-18) fatty acids and had a higher specific activity of the enzyme N-acetylating p-aminohippurate (N-acetyltransferase) than those of uncastrated rats. Thus, castration seems to alleviate some renal effects of the Goldblatt hypertension. In all animals the clamped kidney contained more hydroxyproline and C-18 fatty acids and had a lower N-acetyltransferase activity than the contralateral untouched organ. These results are in accordance with the theory that renal fatty acid concentration interferes directly with the N-acetyltransferase activity of the kidney. The enhanced hydroxyproline content of the kidneys (nephrosclerosis) inhibits N-acetylation most probably indirectly by raising the tissue concentration of C-18 fatty acids.[1]References
- Effect of castration on the experimental renal hypertension of the rat. Blood pressure, nephrosclerosis, long-chain fatty acids, and N-acetylation of PAH in the kidney. Mályusz, M., Ehrens, H.J., Wrigge, P. Nephron (1985) [Pubmed]
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