Different inhibitory effects of 2,4-dinitrophenol, iodoacetate, and probenecid on renal excretion of p-aminohippurate, cyclopenthiazide, and sulfamethoxypyridazine in rats.
The present study was undertaken to determine whether the renal excretion of drugs can be modified by inhibition of the carrier system for organic acids in vivo. The renal excretion of p-aminohippurate is not influenced by 2,4-dinitrophenol but is reduced by iodoacetate and probenecid. The renal excretion of cyclopenthiazide is decreased by all inhibitors. Rats excrete only a very small portion of the administered dose of sulfamethoxypyridazine. Renal sulfamethoxypyridazine excretion is 3 times higher when the tubular reabsorption is blocked by simultaneous administration of NaHCO3. However, even then only a small portion of the injected dose is excreted. Renal sulfamethoxypyridazine excretion is only reduced by probenecid. This finding can be explained by the reduction of the urine volume. It can be concluded that p-aminohippurate and cyclopenthiazide are renally excreted by tubular secretion, whereas sulfamethoxy-pyridazine is excreted by glomerular filtration.
D000618:Aminohippuric Acids / Q000652:urine*; D000818:Animals; D003518:Cyclopenthiazide / Q000652:urine*; D004140:Dinitrophenols / Q000494:pharmacology*; D004232:Diuretics; D005260:Female; D007461:Iodoacetates / Q000494:pharmacology*; D007678:Kidney Glomerulus / Q000502:physiology; D007684:Kidney Tubules / Q000502:physiology; D011339:Probenecid / Q000494:pharmacology*; D051381:Rats; D049993:Sodium Chloride Symporter Inhibitors / Q000652:urine*; D013421:Sulfamethoxypyridazine / Q000652:urine*
D000618:Aminohippuric Acids; D004140:Dinitrophenols; D004232:Diuretics; D007461:Iodoacetates; D049993:Sodium Chloride Symporter Inhibitors; D011339:Probenecid; D013421:Sulfamethoxypyridazine; D003518:Cyclopenthiazide