Sodium nitroprusside excretion

The cyanide nitroprusside test determines the presence of free sulfhydryl or disulfide compounds in urine samples [1, 3,4]. During the first step of the assay, cyanide reduces any disulfides that are present to free sulfhydryl compounds. In the second step, a reddish color reaction results when the free sulfhydryl groups complex with nitroprusside. A positive result is most usually due to cystine in the urine. Familial cystinuria is among the most common aminoacidurias. Disulfides are also excreted in other metabolic disorders such as homo cystinuria and ji-m e reap lol ac la le - cy s lei ne disulfiduria. Both will also produce positive results according to the following reaction RSH + Na2Fe(CN)5NO (sodium nitroprusside) — chromophore + NO. 

ABSORPTION, METABOLISM, AND EXCRETION Sodium nitroprusside is unstable and decomposes under strongly alkaline conditions or when exposed to light. It must be given by continuous intravenous infusion to be effective. Its onset of action is within 30 seconds the peak hypotensive effect occurs within 2 minutes, and the effect disappears within 3 minutes after the infusion is stopped. 

Thiocyanate [SCN ], the anion of thiocyanic acid, is an important waste product from the chemical industry, it is present in various food items, it may be added to dairy milk to promote bacteriostatic processes, and it is synthesixed in the human liver as part of detoxification of cyanide. A special case in medicine has been generation of large amounts of thiocyanate leading to hypothyroidism after sodium nitroprusside infusion for hypertension (Nourok et at, 1964). After oral ingestion thiocyanate is readily absorbed. It is partly bound to albumin in blood, and mainly eliminated by excretion in urine. The half life of thiocyanate in humans is in the order of 1—2 weeks (Scherer, 2006), but varies between individuals. Thiocyanate may have a number of... 

ANF has potent effects on cyclic GMP (cGMP) levels. In vitro, addition of atrial extracts to minced kidney tissue or to primary kidney cell cultures results in increased levels of cGMP.H Injection into anesthetized rats resulted in a 4-fold increase in plasma cGMP levels and a 28-fold increase in urinary excretion.Sodium nitroprusside also causes increased cGMP levels in treated tissues, but probably acts directly through stimulation of guanylate cyclase. Further studies must be done to clarify the role of cGMP in the vasorelaxant and the natriuretic actions of ANF. 

Sodium nitroprusside undergoes a redox reaction that releases cyanide (6,9). The cyanide that is produced is rapidly converted into thiocyanate in the liver by the enzyme thiosulfate sulfotransferase (rhodanase) and is excreted in the urine (6,9). The rate-limiting step in the conversion of cyanide to thiocyanate is the availability of sulfur donors, especially thiosulfate. Toxic symptoms of thiocyanate begin to appear at plasma thiocyanate concentrations of 50 to 100 mg/mL. The elimination half-life of thiocyanate is 2.7 to 7.0 days when renal function is normal but longer in patients with impaired renal function. 

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