Testing Information

Testing Status of Agents at NTP

CAS Registry Number: 7647-14-5 Toxicity Effects

Print this page Easy Link

http://ntp.niehs.nih.gov/go/24212

Selected toxicity information from HSDB, one of the National Library of Medicine's databases. 1

Names (NTP)

  • Sodium chloride
  • IODIZED SALT

Human Toxicity Excerpts

  • SIGNS AND SYMPTOMS: The GI effects of oral salt administration include swollen tongue, nausea, vomiting, diarrhea, abdominal cramps, and thirst. Neurologic effects include thirst, irritability,weakness, headache, convulsions, and coma. Cerebral edema may occur, and muscle tremors may be notes. Cardiovascular manifestations of acute hypernatremia include both hypertension and hypotension. Tachycardia, cardiac failure, and peripheral edema may develop. Pulmonary edema and respiratory arrest may occur. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1058]
  • SIGNS AND SYMPTOMS: Sodium chloride at concentrations much above that in tears causes a stinging sensation on contact with the eye. Solutions up to 10% do not alter the permeability of the corneal epithelium, but solutions more dilute than 0.9% sodium chloride cause increased permeability. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 830]
  • SIGNS AND SYMPTOMS: Hypertonic salt solutions can produce ... a distinctive microscopic lesion of the kidney ... parenchymatous dehydration produces a shrinking which is most conspicuous in the convoluted tubules of the renal cortex. Some experimental evidence suggests that similar hypernatremic syndromes may be produced with normal salt diets if water intake is restricted. [Gosselin, R.E., R.P. Smith, H.C. Hodge. Clinical Toxicology of Commercial Products. 5th ed. Baltimore: Williams and Wilkins, 1984., p. II-126]
  • SIGNS AND SYMPTOMS: Oral administration of concentrated salt solutions causes irritation of the orogastric mucosa. Acute systemic salt poisoning produces CNS damage when brain cells become dehydrated after the acute osmotic shift of intracellular fluids to the extracellular space. Brain cell damage may also occur after idiogenic osmoles have been established and vigorous therapeutic hydration leads to cerebral edema. This may result in a diffuse encephalopathy with multiple small hemorrhages or thromboses. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1058]
  • SIGNS AND SYMPTOMS: The rare inadvertent intravascular administration or rapid intravascular absorption of hypertonic sodium chloride can cause a shift of tissue fluids into the vascular bed, resulting in hypervolemia, electrolyte disturbances, circulatory failure, pulmonary embolism, or augmented hypertension. [Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2006., p. ]
  • SIGNS AND SYMPTOMS: Amniotic fluid embolism or electrolyte imbalance, including hypernatremia, when caused by inadvertent intravascular, myometrial, or intraperitoneal administration of hypertonic sodium chloride, may lead to myometrial necrosis, cortical necrosis of the kidneys, cerebral or pulmonary embolism, hemorrhage with or without disseminated intravascular coagulation, cardiovascular collapse, seizures, and death . Instillation should be discontinued immediately. [Thomson/Micromedex. Drug Information for the Health Care Professional. Volume 1, Greenwood Village, CO. 2006., p. ]
  • SIGNS AND SYMPTOMS: Subconjunctival injection of hypertonic sodium chloride solutions has long been known to cause hyperemia and a transitory rise of intraocular pressure in ... human eyes. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 830]
  • SIGNS AND SYMPTOMS: Salt poisoning increases both the plasma sodium concentration and total sodium in the body ... In addition, salt poisoning impairs the kidney's ability to excrete excess solute. Vacuolization of renal tubular cells and acute tubular necrosis may occur ... The combination of brain shrinkage and distention of intracranial blood vessels associated with the increase in blood volume can result in intraventricular hemorrhage, capillary thrombosis and brain hemorrhage. [Haddad, L.M. and Winchester, J.F. Clinical Management of Poisoning and Drug Overdosage. Philadelphia, PA: W.B. Saunders Co., 1983., p. 681]
  • SIGNS AND SYMPTOMS: The toxicity of NaCl is so low that only mild nasal irritation is experienced by drillers in salt mines even when dust levels exceed the nuisance dust ACGIH TLV of 10 mg/cu m. The main systemic effect of excess NaCl intake is on blood pressure elevation. The lowest toxic dose (TDLO) for an adult man with normal blood pressure is 8.2 g/kg ... [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:785]
  • CASE REPORTS: An estimated dose of more than 400 mEq/kg resulted in brain injuiy and death in a 2 year old child given a salt water solution to induce emesis. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1057]
  • CASE REPORTS: Metabolic acidosis has been reported in an infant who received formula reconstituted with a hypertonic salt solution (sodium, 396 mEq/L). [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1058]
  • ALTERNATIVE and IN VITRO TESTS: The relevance of the pulsed field gel electrophoresis (PFGE) assay for the estimation of the DNA damaging effects of chemicals was studied. Four chemicals were randomly chosen from the list of 50 Multicentre Evaluation of In Vitro Cytotoxicity (MEIC) reference chemicals with known human acute systemic toxicity: acetylsalicylic acid, paracetamol, ethylene glycol and sodium chloride. Human fibroblasts (VH-10) were used as a model system. For the estimation of cytotoxic effect, cell monolayers were treated with chemicals for 24 hours. Cloning efficiency (colony-forming ability) at different concentrations of the test chemicals was estimated, and the 50% inhibitory concentration (IC50) was determined. The IC50 values obtained demonstrated a correlation with human lethal blood concentrations. The induction of DNA double-strand breaks, measured by PFGE as the fraction of activity released, was detected after treatment with paracetamol. However, the other three chemicals tested mainly induced DNA degradation. [Markova E et al; Altern Lab Anim 31 (3): 283-8 (2003) ] PubMed Abstract

Back to Top

Non-Human Toxicity Excerpts

  • LABORATORY ANIMALS: Acute Exposure: Sodium chloride at concentrations much above that in tears causes a stinging sensation on contact with the eye. Solutions up to 10% do not alter the permeability of the corneal epithelium, but solutions more dilute than 0.9% sodium chloride cause increased permeability. On rabbit eyes continuous irrigation for three hr with sodium chloride solutions from 0.3 to 0.6 M and pH 6.0 to 8.0 has produced no morphologic change in the corneas. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 830]**PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Intracarotid injection of 2 M sodium chloride solution in cats rapidly produces cataract on the same side. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 830]**PEER REVIEWED**
  • LABORATORY ANIMALS: Acute Exposure: Subconjunctival injection of hypertonic sodium chloride solutions has long been known to cause hyperemia and a transitory rise of intraocular pressure in rabbit ... eyes. [Grant, W.M. Toxicology of the Eye. 3rd ed. Springfield, IL: Charles C. Thomas Publisher, 1986., p. 830]**PEER REVIEWED**
  • LABORATORY ANIMALS: Subchronic or Prechronic Exposure: Rats given sodium chloride at 2.8-9.8% in diet rations develop hypertension within a few weeks or months. When unselected rats are used in such experiments, the incidence and severity of hypertension vary directly with the sodium chloride concentration in the diet. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 401]**PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Effects of sodium chloride and ethanol on gastric tumor development in rats after treatment with N-methyl-N-nitro-N-nitrosoguanidine were studied. N- methyl-N-nitro-N-nitrosoguanidine, dissolved in distilled water (5 g/L), was administered orally once by gastric tube at a dose of 0.25 mL/10 g body wt to 4 wk old ACI rats. After this carcinogen initiation, animals were fed on a diet containing 10% sodium chloride (Group 2) or normal diet with 10% ethanol in the drinking water (Group 4). N-methyl-N-nitro-N-nitrosoguanidine alone (Group 1), sodium chloride alone (Group 3), ethanol alone (Group 5), and control (Group 6) animals were also maintained. All survivors were killed one year after the N-methyl-N-nitro-n-nitrosoguanidine application. Incidences of tumors in the forestomach and glandular stomach were significantly increased in Group 2 as compared to Group 1 (p< 0.05). The height of the pyloric mucosa was significantly greater in Group 2 than in Groups 4, 5 or 6 (p< 0.05). In the fundic area, the mucosal height was significantly decreased in Group 4 as compared to Group 6 (p< 0.05). The present results demonstrate that whereas tumors in the glandular stomach and forestomach are both promoted by sodium chloride, ethanol is without influence. Furthermore, sodium chloride, a promoter of glandular stomach tumorigenesis also increases cell proliferation. [Watanabe H et al; Jpn J Cancer Res 83 (6): 588-93 (1992) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Chronic Exposure or Carcinogenicity: Effects were studied of sodium chloride on production of gastric carcinomas by 4-nitroquinoline-1-oxide in male Wistar rats. NaCl given alone had no apparent carcinogenicity but when admin with 4-nitroquinoline-1-oxide it enhanced carcinogenic effects in stomach. [TATEMATSU M ET AL; J NATL CANCER INST 55 (1): 101 (1975) ]**PEER REVIEWED**
  • LABORATORY ANIMALS: Developmental or Reproductive Toxicity: 1900 or 2500 mg/kg was injected into mice on the 10th or 11th day of pregnancy and produced up to 18% skeletal defects. Clubfoot was the most frequently found defect. The type of defect was different than that found with fasting. [Shepard, T.H. Catalog of Teratogenic Agents. 5th ed. Baltimore, MD: The Johns Hopkins University Press, 1986., p. 521]**PEER REVIEWED**
  • GENOTOXICITY: Genotoxic stress triggers a variety of biological responses including the transcriptional activation of genes regulating DNA repair, cell survival and cell death. Genomic approaches, which monitor gene expressions across large numbers of genes, can serve as a powerful tool for exploring mechanisms of toxicity. Here, ... five different agents ../were/ investigated to determine/ whether the analysis of genome-wide expression profiles in Saccharomyces cerevisiae could provide insights into mechanisms of genotoxicity versus cytotoxicity. To differentiate the genotoxic stress-associated expression signatures from that of a general cytotoxic stress, /the authors/ compared gene expression profiles following the treatment with DNA-reactive (cisplatin, MMS, bleomycin) and DNA non-reactive (ethanol and sodium chloride) compounds. Although each of the tested chemicals produced a distinct gene expression profile, we were able to identify a gene expression signature consisting of a relatively small number of biologically relevant genes capable of differentiating genotoxic and cytotoxic stress. The gene set includes such upregulated genes as HUG1, ECM4 and previously uncharacterized gene, YLR297W in the genotoxic and GAP1, CGR1 in the cytotoxic group. /The/ results indicate the potential of gene expression profile analysis for elucidating mechanism of action of genotoxic agents. [Caba E et al; Mutat Res 575 (1-2): 34-46 (2005) ]**PEER REVIEWED** PubMed Abstract
  • OTHER TOXICITY INFORMATION: During the first 48 hr /of salt toxicity/, swine develop eosinopenia, eosinophilic cuffs around vessels in the cerebral cortex and adjacent meninges, and cerebral edema or necrosis. After 3-4 days, eosinophilic cuffs are usually no longer present. The GI mucosa may be inflamed and congested and may have pinpoint, blood-filled ulcers. Cattle do not have eosinophilic cuffs; they have gastric inflammation or ulceration (or both), edema of skeletal muscles, and hydropericardium. Chickens have hydropericardium. In acute cases, no gross lesions may be present in any species. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In cases of salt poisoning in ruminants there is usually a history of salt hunger. Deaths of 15 out of 18 dairy cattle were attributed to over indulgence in rain wetted salt following a dry period of three weeks during which the salt had become too hard to be edible ... Although the toxic dose of common salt for sheep and cattle is very high, salt hungry animals may consume too much, especially when loose salt is offered to them: mineral licks are obviously safer ... Treatment of salt poisoning is largely non-specific. Fresh, salt free water should be made available as soon as possible. [Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 40]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In the field, instances are numerous in which deaths in pigs have followed suddenly upon feeding swill which has been found subsequently to contain large amounts of sodium chloride. The source of the salt is commonly waste from bake houses, pickling and canning factories and the like. One case was reported in which a whole litter of pigs died after being given a meal of the sweepings from a tarpaulin on which the ration had been previously mixed. The sweepings contained over 23% salt. In other cases spilled salt and even sweepings from paths on to which salt has been sprinkled to melt snow have found their way into swill. [Clarke, M. L., D. G. Harvey and D. J. Humphreys. Veterinary Toxicology. 2nd ed. London: Bailliere Tindall, 1981., p. 40]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In selective breeding experiments, sodium sensitive and sodium resistant strains can be produced by inbreeding separately rats that do and rats that do not develop hypertension in response to sodium chloride. Among genetically sodium sensitive rats, young animals are more sensitive to the effects of sodium than adults. When hypertension becomes established in these animals, it is not corrected by reducing sodium intake. Despite many generations of inbreeding, the sodium sensitive animals will maintain normal blood pressure throughout life if they are never exposed to excessive intake of sodium. [National Research Council. Drinking Water & Health Volume 1. Washington, DC: National Academy Press, 1977., p. 404]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Salt toxicity (sodium chloride, NaCl), which is more appropriately called “water deprivation sodium ion toxicosis” can result when excessive quantities of salt are ingested and intake of potable water is limited. Salt toxicity is unlikely to occur as long as salt-regulating mechanisms are intact and fresh drinking water is available. It has been reported in virtually all species of animals all over the world. In the USA, it is more common in swine (the most sensitive species), cattle, and poultry. Sheep are relatively resistant. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2514]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Salt toxicity is directly related to water consumption. Water intake in animals can be reduced significantly or abolished completely due to factors such as mechanical failure of waterers, overcrowding, unpalatable medicated water, new surroundings, or frozen water. ... [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Feeder pigs on feed containing only 0.25% salt have had salt poisoning when water intake was limited, yet even 13% salt in feed may not produce poisoning when adequate fresh water is consumed. Swine feed should contain 0.5-1% salt, and fresh drinking water should always be available. Feeding whey or brine containing 3-4% salt can result in toxicosis in most livestock and poultry species. Similarly, ingestion of 1-3 kg of salt in deprived animals can result in salt toxicosis even when water is available, especially in cattle. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Chickens can tolerate up to 0.25% salt in drinking water but are susceptible to sodium ion toxicosis when water intake is restricted. Wet mash containing 2% salt caused poisoning in ducklings. High salt content in wet mash is more likely to cause poisoning than in dry feed, probably because birds eat more wet mash. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: Cattle and sheep on range can develop salt poisoning when a high percentage of mineral supplement is provided, and the water supply is limited or saline. Sheep can tolerate 1% salt in drinking water; however, 1.5% may be toxic. It is generally recommended that drinking water should contain <0.5% total salt for any species of livestock. Chronic salt poisoning in cattle can cause gastroenteritis, depressed appetite, weight loss, and dehydration. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In pigs, early signs /of salt toxicity/ (rarely seen) may be increased thirst, pruritus, and constipation. Affected pigs may be blind, deaf, and oblivious to their surroundings; they will not eat, drink, or respond to external stimuli. They may wander aimlessly, bump into objects, circle, or pivot around a single limb. After 1-5 days of limited water intake, intermittent seizures occur with the pig sitting on its haunches, jerking its head backward and upward, and finally falling on its side in clonic-tonic seizures and opisthotonos. Terminally, pigs may lie on their sides, paddling in a coma, and die within a few to 48 hr. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In cattle, signs of acute salt poisoning involve the GI tract and CNS. Salivation, increased thirst, vomiting (regurgitation), abdominal pain, and diarrhea are followed by ataxia, circling, blindness, seizures, and partial paralysis. Cattle sometimes manifest belligerent and aggressive behavior. A sequela of salt poisoning in cattle is dragging of hindfeet while walking or, in more severe cases, knuckling of the fetlock joint. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**
  • OTHER TOXICITY INFORMATION: In poultry, increased thirst, dyspnea, fluid discharge from the beak, weakness, diarrhea, and leg paralysis are some of the common signs of salt poisoning. [Kahn, C.M. (Ed.); The Merck Veterinary Manual 9th ed. Merck & Co. Whitehouse Station, NJ. 2005, p. 2515]**PEER REVIEWED**

Back to Top

Human Toxicity Values

  • The estimated fatal dose of sodium chloride is approximately 0.75 to 3.00 g/kg. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1057]**PEER REVIEWED**

Back to Top

Non-Human Toxicity Values

  • LD50 Rat oral 3000 mg/kg [ITII. Toxic and Hazarous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1982., p. 472]**PEER REVIEWED**
  • LD50 Mouse ip 2602 mg/kg [ITII. Toxic and Hazarous Industrial Chemicals Safety Manual. Tokyo, Japan: The International Technical Information Institute, 1982., p. 472]**PEER REVIEWED**
  • LD50 Mouse oral 4000 mg/kg [Kirk-Othmer Encyclopedia of Chemical Technology. 3rd ed., Volumes 1-26. New York, NY: John Wiley and Sons, 1978-1984., p. V15 581 (1981)]**PEER REVIEWED**

Back to Top

Absorption, Distribution and Excretion

  • The primary route of sodium excretion is the urine; additional excretion occurs in sweat and feces. The kidney filters sodium a the glomerulus, but 60% to 70% is reabsorbed in the proximal tubules along with bicarbonate and water. Another 25% to 30% is reabsorbed in the loop of Henle, along with chloride and water. In the distal tubules, aldosterone modulates the reabsorption of sodium and, indirectly, chloride. The renal threshold for sodium is 110 to 130 mEq/L. Less than 1% of the filtered sodium is excreted in the urine. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1057]**PEER REVIEWED**
  • Sodium is rapidly absorbed from the GI tract; it is also absorbed from rectal enemas. Intestinal wall absorption occurs via the Na+, K+-adenosine triphosphatase system that is augmented by aldosterone and desoxycorticosterone acetate. Sodium is not bound by plasma proteins. The volume of distribution is 0.64 L/kg. [Dart, R.C. (ed). Medical Toxicology. Third Edition, Lippincott Williams & Wilkins. Philadelphia, PA. 2004., p. 1057]**PEER REVIEWED**
  • In one study using radiolabeled 20% sodium chloride injection, most of the drug concentrated in the decidua and the fetal part of the placenta following intra-amniotic injection. Following intra-amniotic administration of 20% sodium chloride injection, some of the drug diffuses into the maternal blood. [McEvoy, G.K. (ed.). American Hospital Formulary Service. AHFS Drug Information. American Society of Health-System Pharmacists, Bethesda, MD. 2006., p. 3215]**PEER REVIEWED**
  • Atrichial sweat glands ... are the organs by which considerable body water and electrolytes, mainly sodium chloride, are lost. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 8:69]**PEER REVIEWED**
  • Sweating causes loss of both body water and electrolytes, especially sodium chloride, but only in diluted proportion to body fluids. Because sweat produced by atrichial glands is hyposmotic, sweating has the net effect of depleting body water, more than its electrolytes. Prolonged heavy sweating, however, challenges both. [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 8:89]**PEER REVIEWED**
  • ... Sodium ... ion is the principal electrolyte in extracellular fluid, which is excreted in the urine. /Na+/ [Bingham, E.; Cohrssen, B.; Powell, C.H.; Patty's Toxicology Volumes 1-9 5th ed. John Wiley & Sons. New York, N.Y. (2001)., p. 3:590]**PEER REVIEWED**
  • Angiotensin II has pronounced effects on renal function to reduce the urinary excretion of Na+ and water while incr the excretion of K+ ... Very low concn of angiotensin II stimulate Na+/H+ exchange in the proximal tubule--an effect that incr Na+, Cl-, and bicarbonate reabsorption ... At high concn, angiotensin II may inhibit Na+ transport in the proximal tubule ... Angiotensin II stimulates the zona glomerulosa of the adrenal cortex to incr the synthesis and secretion of aldosterone ... Aldosterone acts on the distal and collecting tubules to cause retention of Na+ and excretion of K+ and H+. The stimulant effect of angiotensin II on the synthesis and release of aldosterone is enhanced under conditions of hyponatremia or hyperkalemia and is reduced when concn of Na+ and K+ in plasma are altered in the opposite direction. Such changes in sensitivity are due in part to alterations in the number of receptors for angiotensin II on zona glomerulosa cells as well as to adrenocortical hyperplasia in the Na+-depleted state ... Reductions in renal blood flow markedly attenuate renal excretory function, and angiotensin II reduces renal blood flow by directly constricting the renal vascular smooth muscle, by enhancing renal sympathetic tone (a CNS effect), and by facilitating renal noradrenergic neurotransmission (an intrarenal effect) ... Angiotensin II may reduce Na+ excretion in part by diminishing medullary blood flow. /Na+/ [Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 818]**PEER REVIEWED**
  • Arterial blood pressure is a major determinant of Na+ excretion ... The renin-angiotensin system plays a major role in maintaining a constant ... levels of arterial blood pressure despite extreme changes in dietary Na+ intake. When dietary Na+ intake is low, renin release is stimulated, and angiotensin II acts on the kidneys ... Conversely, when dietary Na+ is high, renin release is inhibited ... /causing/ the withdrwal of angiotensin II ... /Na+/ [Hardman, J.G., L.E. Limbird, P.B., A.G. Gilman. Goodman and Gilman's The Pharmacological Basis of Therapeutics. 10th ed. New York, NY: McGraw-Hill, 2001., p. 818]**PEER REVIEWED**

Back to Top

Metabolism/Metabolites

  • None found

Back to Top

TSCA Test Submissions

  • None found

Back to Top

Footnotes

1 Source: the National Library of Medicine's Hazardous Substance Database, 10/28/2007.

Back to top

Web page last updated on May 14, 2008