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)

Primary peripheral arterial vasodilation with relative underfilling of the arterial circulation occurs in early pregnancy and leads to several consequences, including decreased systolic and diastolic blood pressures, enhanced cardiac output secondary to afterload reduction, stimulation of the renin-angiotensin-aldosterone axis, nonosmotic stimulation of thirst and vasopressin release, and renal sodium and water retention with expansion of the extracellular fluid and plasma volume compartments. These are events known to occur in all states of arterial vasodilation. Pregnancy has, however, several unique features. Primary arterial vasodilation generally is associated with no change or a decrease in renal blood flow and glomerular filtration rate and failure to escape from the sodium-retaining effects of aldosterone. In early pregnancy, renal blood flow and glomerular filtration rate increase by 30-50% in parallel with the peripheral arterial vasodilation but before plasma volume expansion. No known vasodilator exhibits such a profound effect on renal hemodynamics. Vasodilating prostaglandins may contribute to, but cannot explain, this remarkable enhancement of renal hemodynamics in early pregnancy. Therefore, a highly potent, as yet undefined, systemic and renal vasodilator must be unique to pregnancy. The increased glomerular filtration rate and filtered sodium load with enhanced distal tubular sodium delivery allows escape from aldosterone, an effect not observed in other states of arterial underfilling. This vasodilator may also account, at least in part, for the vascular resistance to angiotensin known to occur in normal pregnancy. This hypothesis for the normal physiology of pregnancy sets the stage for understanding the pathogenesis of preeclampsia-eclampsia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral arterial vasodilation hypothesis of sodium and water retention in pregnancy: implications for pathogenesis of preeclampsia-eclampsia. 206 82

We report a female patient presenting with sepsis and multi-organ failure following eclampsia and intrauterine childdeath. In the phase of recovery, the patient developed consciousness disorder and coma characterized by fasciculation, generalized myoclonia and respiratory insufficiency. The clinical picture corresponded to that of Lance Adam's syndrome. A quick change in the composition of body fluids in the polyuric phase of renal insufficiency associated with an antidiuretic hormone deficit was a cause of that disorder. Metabolic dysfunction and hyperexcitability of neurons developed as a result. Hyperexcitability of the caudal part of the medulla oblongata was responsible for the development of myoclonia. Following the correction of that disorder, the patient completely improved.
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PMID:[Disorders of consciousness due to disorders of body fluid composition--case report of a female patient]. 864 63

The renal handling of urate involves complete glomerular filtration followed by reabsorption and secretion mainly in the proximal renal tubule. The amount of urate excreted depends on the extracellular fluid volume. Expansion of extracellular fluid volume increases and contraction of extracellular fluid volume decreases the clearance of urate. In the syndrome of inappropriate secretion of antidiuretic hormone, there is volume expansion associated with low uric acid. A comparable situation is observed whenever exaggerated amounts of free water are consumed. Similarly, hypouricaemia and a tendency to low serum sodium concentrations are observed in normal pregnancy, a state with volume expansion, a physiological situation reversed when eclampsia occurs. On the other hand, when hyponatraemia is associated with contraction of extracellular fluid volume as it is often the case when thiazides or loop-diuretics are administered, hyponatraemia is paralleled by increased serum uric acid concentrations.
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PMID:[Serum concentration of uric acid, a diagnostic 'must' in patients with hyponatremia]. 1549 21

Posterior reversible encephalopathy syndrome (PRES) is a clinicoradiological entity characterized by a typical brain edema. Its pathogenesis is still debated through hypoperfusion and hyperperfusion theories, which have many limitations. As PRES occurs almost exclusively in clinical situations with arginine vasopressin (AVP) hypersecretion, such as eclampsia and sepsis, we hypothesize that AVP plays a central pathophysiologic role. In this review, we discuss the genesis of PRES and its symptoms through this novel approach. We theorize that AVP axis stimulation precipitates PRES development through an increase in AVP secretion or AVP receptor density. Activation of vasopressin V1a receptors leads to cerebral vasoconstriction, causing endothelial dysfunction and cerebral ischemia. This promotes cytotoxic edema through hydromineral transglial flux dysfunction and may increase endothelial permeability, leading to subsequent vasogenic brain edema. If our hypothesis is confirmed, it opens new perspectives for better patient monitoring and therapies targeting the AVP axis in PRES.
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PMID:Arginine Vasopressin and Posterior Reversible Encephalopathy Syndrome Pathophysiology: the Missing Link? 3092 75