Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electrolyte abnormalities are a frequent and potentially hazardous complication in patients with heart failure. This may be due to the pathophysiological alterations seen in the heart failure state leading to neurohumoral activation (stimulation of the renin-angiotensin-aldosterone system, sympathoadrenergic stimulation), and due to the complications of therapy with diuretics, cardiac glycosides or ACE inhibitors. Patients with heart failure may exhibit hyponatremia due to a decrease in water excretion, which may be related to the enhanced release of both angiotensin and vasopressin and can be exaggerated by diuretic therapy. Along with potassium and calcium, magnesium influences cardiovascular function. Magnesium and potassium deficiencies play an important role in the development of cardiac arrhythmias. Magnesium is essential for the maintenance of intracellular potassium concentration. Although there are conflicting data regarding the prevalence of hypomagnesemia in patients with chronic heart failure (the values range from 7-37%), multiple studies have documented lower magnesium concentrations in patients with heart failure than in normal controls. As magnesium and potassium are mainly intracellular ions, measurements in serum or plasma are of limited value to assess magnesium status. There was no correlation between the intracellular electrolyte content and the electrolyte levels in plasma, either for mononuclear cells or erythrocytes or for myocardial and skeletal muscle. Loop diuretics (e.g. furosemide) are supposed to cause a substantial loss of both magnesium and potassium in the plasma and intracellular space. The potassium-sparing diuretics amiloride and triamterene are reported to also exert magnesium-sparing effects. Recently, ACE inhibitors have been documented to have important magnesium-conserving actions, possibly via their effect on glomerular filtration. Hyperkalemia, secondary to the use of ACE inhibitors in patients with heart failure, is well documented. Digoxin directly limits the renal tubular reabsorption of magnesium, therefore increasing magnesium excretion. Low magnesium and potassium concentrations increase cardiac glycoside toxicity. In contrast, elevated levels of magnesium decrease the sensitivity of human myocardium to antiarrhythmogenic actions of cardiac glycosides, without affecting maximally developed tension. Moreover, magnesium increases binding affinity of cardiac glycosides to the receptor. The antiarrhythmic action of magnesium is suspected to be mediated by a reduced sensitivity to electrophysiological changes induced by Ca2+, thus indicating Ca2+ antagonistic properties of magnesium. Magnesium deficiency has also been implicated in sudden death, notably in patients with congestive heart failure. Therefore, when treating congestive heart failure, one must consider how to prevent depletion of electrolytes or how to replete potassium and magnesium in deficiency states.
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PMID:Heart failure and electrolyte disturbances. 150 35

The mammalian renal thick ascending limb of Henle (TAL) reabsorbs approximately 55% of the filtered magnesium; accordingly, it is the major segment involved in control of renal Mg balance. This review discusses recent evidence for passive and active transport of Mg through the paracellular and transcellular pathways of the TAL, respectively. The properties of these pathways provide a basis for understanding the factors influencing magnesium reabsorption and hormonal controls regulating Mg balance. Normally, Mg absorption is load dependent, whether delivery is altered by increasing luminal Mg concentration or increasing the flow rate into the thick ascending limb. In contrast to the luminal concentration, elevation of peritubular (plasma) Mg and Ca inhibit divalent cation absorption by mechanisms that are not entirely clear. Magnesium reabsorption in the TAL is also closely associated with NaCl absorption so that factors that influence NaCl also affect magnesium. Magnesium deficiency results in a specific and apparently intrinsic cellular adaptation to increase Mg absorption in the TAL. Our greatest understanding of hormonal controls for Mg absorption have come from recent studies using a "hormone deprived" animal model. Parathyroid hormone, calcitonin, glucagon, and antidiuretic hormone act through a common second messenger, adenosine 3',5'-cyclic monophosphate, to limit Mg excretion by enhancing active Mg transport in the TAL. The integrated actions of these hormones and possibly others provide a sensitive means of control. Clearly, recent observations, using in vivo and in vitro microperfusion studies, have altered our thinking of TAL function and indicate that Mg transport is sensitively and specifically controlled within this segment.
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PMID:Control of magnesium transport in the thick ascending limb. 264 45