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• Exogenous vasopressin elicits all the pharmacologic responses usually produced by endogenous vasopressin (antidiuretic hormone); primary physiologic role of vasopressin is to maintain serum osmolality within a normal range.
• Produces relatively concentrated urine by increasing reabsorption of water by the renal tubules. Its action in regulating body fluid balance is mediated by renal vasopressin V₂ receptors, which are coupled to adenyl cyclase and the generation of cyclic AMP. At the tubular level, vasopressin stimulates adenyl cyclase activity, leading to increases in cyclic adenosine monophosphate (AMP). Cyclic AMP increases water permeability at the luminal surface of the distal convoluted tubule and collecting duct, resulting in increased urine osmolality and decreased urinary flow rate.
• Conserves up to 90% of the water that might otherwise be excreted in the urine. Vasopressin also increases reabsorption of urea by the collecting ducts.
• Increases coronary blood flow and the availability of oxygen to the myocardium. A preferred approach in patients with asystolic cardiac arrest would be to administer vasopressin rather than epinephrine initially, reserving epinephrine for patients who do not experience ROSC with the initial vasopressin doses.
• In doses greater than those required for antidiuretic effects, vasopressin directly stimulates contraction of smooth muscle V₁ receptors.
• The vasoconstrictive action of vasopressin is mediated by vascular V₁ receptors; the vascular receptors are coupled to phospholipase C, resulting in release of calcium from sarcoplasmic reticulum in smooth muscle cells, leading to vasoconstriction.
• Causes vasoconstriction, particularly of capillaries and of small arterioles, resulting in decreased blood flow to the splanchnic, coronary, GI, pancreatic, skin, and muscular systems.
• When administered into the celiac or superior mesenteric arteries, vasopressin constricts gastroduodenal, left gastric, superior mesenteric, and splenic arteries; however, hepatic arteries are not constricted and, instead, hepatic blood flow often increases.
• In the intestinal tract, increases peristaltic activity, particularly of the large bowel; also causes an increase in GI sphincter pressure and a decrease in gastric secretion but has no effect on gastric acid concentration. Contraction of smooth muscle of the gallbladder and of the urinary bladder also occurs.
• Oxytocic properties of vasopressin are minimal, but in large doses the drug may stimulate uterine contraction. The hormone also possesses slight milk ejecting properties but its role during lactation is negligible.
• In addition to its peripheral effects, vasopressin causes release of corticotropin, growth hormone, and follicle-stimulating hormone.

Advice to Patients

• Importance of alerting patients that ceratin adverse effects (e.g., blanching of skin, abdominal cramps, nausea) may be reduced by taking 1 or 2 glasses of water at the time of administration. These side effects are usually not serious and probably will disappear within a few minutes.
• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs.
• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.
• Importance of informing patients of other important precautionary information. (See Cautions.)

Preparations

AHFS Drug Information. © Copyright, 1959-2008, Selected Revisions July 2007. American Society of Health-System Pharmacists, Inc., 7272 Wisconsin Avenue, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

Remember, keep this and all other medicines out of the reach of children, never share your medicines with others, and use this medication only for the indication prescribed.