Minireview: physiological and pharmacological properties of vanadium.
Vanadium is distributed extensively in nature. It is a trace element and is present in almost all living organisms including man. Even though vanadium was originally recognized for its ability to inhibit membrane Na+-K+-ATPase, various laboratory studies now document that this element has the capacity to affect the activity of various intracellular enzyme systems and may modify their physiological functions. Vanadium may be an essential element for normal development and may play an important role in various homeostatic mechanisms, and thus vanadium deficiency may prove to be an important concern. Abnormalities in biological disposition of vanadium may be involved in the pathogenesis of certain neurological disorders or cardiovascular diseases. While the essentiality of this element for living organisms is yet to be established with certainty, vanadium has become an increasingly important element and is used extensively in various heavy industries such as steel, oil, etc.; thus, the incidence of exposure to toxic levels of vanadium to industrial workers has been an increasing concern for toxicologists. To date, little information is available on the physiological or pharmacological actions of vanadium; hence, it is difficult to reach any definitive conclusion concerning its biological significance, essentiality and its role in pathological states. An attempt has been made in this review to broadly document what is known of various biological actions of vanadium.
D000818:Animals; D001692:Biological Transport / Q000187:drug effects; D001714:Bipolar Disorder / Q000209:etiology; D002118:Calcium / Q000378:metabolism; D000252:Calcium-Transporting ATPases / Q000037:antagonists & inhibitors; D002319:Cardiovascular System / Q000187:drug effects; D002490:Central Nervous System / Q000187:drug effects; D006801:Humans; D006973:Hypertension / Q000209:etiology; D007473:Ion Channels / Q000187:drug effects / Q000378:metabolism; D007668:Kidney / Q000187:drug effects; D009119:Muscle Contraction / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D000254:Sodium-Potassium-Exchanging ATPase / Q000037:antagonists & inhibitors; D014638:Vanadates; D014639:Vanadium / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology* / Q000633:toxicity; D014661:Vasoconstriction / Q000187:drug effects
D007473:Ion Channels; D014639:Vanadium; D014638:Vanadates; D000252:Calcium-Transporting ATPases; D000254:Sodium-Potassium-Exchanging ATPase; D002118:Calcium