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)

The rate of urine formation and its composition are influenced by the different drugs used during surgery. Anaesthetics act on renal function, not only directly, but also by producing changes in cardiovascular function and in neuroendocrine activity. Many factors may be incriminated: lowered blood pressure and cardiac output, increased sympathetic outflow (renal nerve stimulation and increased plasma catecholamines), increased release of renin, angiotensin and vasopressin. The effects of anaesthetics on the kidney go beyond a simple change in basal haemodynamics and include, for some drugs, an alteration in the ability for the kidney to autoregulate its blood flow and glomerular filtration rate. Studies on toad bladders showed a decrease in transport of water, sodium and organic anions. But, in fact, renal effects of anaesthetics in man and animals depend on the species, the anaesthetic and the method used to study the effect. Most barbiturates and inhalational anaesthetics tend to decrease renal blood flow (RBF) and glomerular filtration rate (GFR). These trends are gradually reversed during recovery. The effects of ketamine and diazepam are not clearly defined. Morphine and fentanyl decrease urine flow and GFR, whilst RBF increases or decreases, depending on whether a direct or indirect measurement technique was used. Muscle relaxants have little effect on renal function. Spinal and epidural anaesthesia only slightly decrease GFR and RBF in proportion to the decrease in mean arterial pressure. Obviously, the preexisting intravascular volume and the quantity of intravenous fluids given strongly influence the renal response to spinal and epidural anaesthesia. Some studies have shown that urine flow rate, creatinine clearance, urinary sodium excretion and RBF are reduced during mechanical ventilation with positive end-expiratory pressure. Surgery itself influences renal function by inducing alterations in prerenal haemodynamics. Operative stress leads to an increase in circulating catecholamines and angiotensin. Significant fluid shifts, excessive blood loss and redistribution of a third space may lead to a prerenal oliguric state, increasing secretion of vasopressin. Acute renal failure (ARF) is a frequently lethal complication of critical surgical illness, due to a variety of factors which interfere with glomerular filtration and tubular reabsorption, such as renal hypoperfusion or nephrotoxic insults. In fact, the initiating aggression ultimately culminates in the development of one or more of the maintenance factors (decreased tubular function, tubular obstruction, decreased GFR and RBF) that reduce urine flow and osmolar excretion. Good management during the perioperative period tends to minimize the risk of developing ARF.
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PMID:[Changes in renal function induced by anesthesia]. 227 18

Atrial natriuretic factor (ANF) is a humoral agent isolated in recent years from cardiac atrial tissue, and produced by atrial cardiocytes as a peptide precursor containing 152 amino acids. In secretory atrial granules, it is stored in reserve form as a prohormone and released into circulation as a 28-amino acid peptide from the C-terminal portion of the peptide precursor representing the active circulating hormone. ANF possesses potent natriuretic, myorelaxant, vasodilatory and blood pressure-lowering properties. Besides, it inhibits renin, aldosterone and vasopressin secretion. It is present also in the CNS and its function is closely related to the sympathetics nerves. By its direct renal and vascular effect, renin-angiotensin-aldosterone system and vasopressin inhibition and, by its neuromodulatory action on the central and sympathetic nerves, ANF plays an important role in electrolyte, volume and pressure homeostasis. The development of a radioimmunoassay for ANF determination in the plasma of rats and man enabled us to follow up its changes under various experimental conditions (water deprivation, increased or decreased salt intake, effect of anaesthetics, ontogenetic changes in ANF concentration during development of hypertension in the spontaneously hypertensive rat) and in clinical studies (effect of ECV expansion in controls, arterial hypertension, liver cirrhosis as well as ANF changes in congestive heart failure or chronic renal failure). These findings of ours have supported the concept that ANF represents an important adaptive and corrective mechanism mobilized during intravascular volume and blood pressure changes in an effort to normalize these. ANF is expected to find use also in the treatment of oedema, arterial hypertension and acute renal failure.
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PMID:Atrial natriuretic factor and its role in the regulation of electrolyte, volume and pressure homeostasis. 252 70

Water immersion (WI)-induced alterations of circulating plasma volume (PV), plasma renin activity (PRA), plasma levels of aldosterone (Ald), vasopressin (AVP) and atrial natriuretic peptide (ANP) were examined in 12 patients with noninflammatory acute renal failure (ARF) at the anuric/oliguric phase, in 20 hemodialyzed patients with chronic renal failure and in 15 healthy subjects. Patients with acute and chronic renal failure showed significantly elevated basal ANP concentrations (138.67 +/- 12.88 and 295.8 +/- 21.87 pg/ml, respectively) as compared with normals (74.54 +/- 4.1 pg/ml) and significantly elevated PRA (20.85 +/- 3.24 and 6.60 +/- 0.94 ng/ml/h, respectively versus 2.33 +/- 0.31 ng/ml/h), plasma levels of Ald (16.11 +/- 1.26 and 18.11 +/- 1.58 ng/dl, respectively versus 12.71 +/- 1.03 ng/dl) and AVP (6.95 +/- 0.62 and 6.08 +/- 0.54 pg/ml, respectively versus 2.68 +/- 0.48 pg/ml). After 2 hrs of WI a significant decline of PRA, Ald and AVP but an increase of ANP was noted in all examined groups. The absolute WI-induced increase in plasma ANP was significantly less marked in uremic patients than in normals. The endocrine profile of patients with ARF differed only quantitatively from that of patients with CRF both under basal and WI conditions. WI was followed by a significant increase of PV which was significantly more marked in patients with ARF (+ 16.42 +/- 1.73%) than in CRF (10.57 +/- 0.37%) and in normals (+11.3 +/- 1.6%). Only in healthy subjects a significant correlation was found between WI-induced changes of PV and ANP, PRA and Ald, and between PRA and AVP.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Water immersion-induced alterations of plasma atrial natriuretic peptide level and its relationship to the renin-angiotensin-aldosterone system and vasopressin secretion in acute and chronic renal failure. 252 41

ANF is an exciting, newly discovered hormone that has significant potential for furthering our understanding of the complex interactions involved in fluid and electrolyte balance. In addition to effects on water and salt balance, it is a potent vasodilator, as well as inhibitor of renin, angiotensin II, aldosterone, and vasopressin. ANF is primarily produced in the atria, but production in the brain is suggestive of action as a neuropeptide and as a potential regulator of CSF production. Receptors are found throughout the heart, vascular tree, kidney, adrenal gland, and brain. The stimulus for release appears to be atrial stretch, which may be secondary to intravascular fluid changes. It causes hemoconcentration and may be an important regulator of interstitial fluid distribution as well as capillary permeability. Patients with CHF and renal failure have been found to have elevated levels that decrease in response to treatment. Potentially, it may be useful as a therapeutic agent in acute renal failure, CHF and other fluid disturbances. ANF is a testament to the incredible advances in peptide biology. Within 2 years of the discovery, ANF was sequenced and cloned. Since that time, literally thousands of papers describing its actions have been published. Our knowledge about this hormone grows at an exponential rate. It is clear that this hormone is intimately involved in the regulation of fluid and electrolyte balance, vascular tone, and the pathophysiology of CHF but many questions remain unanswered. Continued research will provide many of the missing pieces to this very complex, new hormone system.
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PMID:Atrial natriuretic factor. 252 98

Cortical, medullary and papillary T1 and T2 water proton relaxation times were measured at 37 degrees C, 20 MHz. The measurements were made using kidneys from rats affected by many forms of experimental acute renal failure (ARF), namely acute hemorrhagic hypovolemia, angiotensin II administration, antidiuretic hormone (ADH) administration, glycerol, and other nephrotoxins (gentamicin, cisplatinum, cyclosporine), renal artery occlusion for different periods of time, and ureteral ligation. From the T1 and PW (percent tissue water content) the bound water (FB) and HF (percent water bound/g solid) were calculated according to a fast proton diffusion model. In most experimental models studied, the experiments were repeated following paramagnetic enhancement with GdDTPA administration (70 mmol/kg BW). By profiling the deviations from normal, it was possible to differentiate the ischemic (shortened T1, prolonged T2), obstructive (very high T1 and T2 in both cortex and medulla) and nephrotoxic (prolonged T2) forms of ARF. Significant changes in free/bound water compartments occurred, though their biological significance is unknown. T1 and T2 ratios before and after paramagnetic enhancement correlated well with estimates of glomerular filtration rate. In the first minutes following acute hemorrhagic hypovolemia, the intrarenal water distribution remained unchanged. After GdDTPA significant water proton T1 and T2 changes characterized the immediate posthemorrhagic state similar to the effect of ADH.
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PMID:Renal proton magnetic resonance in experimental acute renal failure in rats. 256 Feb 33

Effects of open-heart surgery on renal function were studied in 38 patients who had uneventful postoperative course with no sign of acute renal failure. Of these, 19 underwent aorto-coronary bypass grafting (Group 1) and 19 underwent valve replacement (Group 2). During cardiopulmonary bypass (CPB), renal plasma flow (RPF) and glomerular filtration rate (GFR) significantly decreased in both groups as compared to the preoperative values. The decreased GFR remained significantly low on the day of operation in both groups and returned to the preoperative level on the 1st postoperative day (POD) in group 1 and on the 3rd POD in group 2. On the other hand, plasma antidiuretic hormone (ADH) level markedly increased during CPB and remained significantly higher than the preoperative level through the 1st POD. Despite the decreased GFR and increased ADH, however, urinary flow markedly increased during CPB in both groups and remained at significantly higher level than the preoperative values through the 3rd POD in group 1 and through the 5th POD in group 2. Fractional excretion of sodium significantly increased during CPB in both groups and remained high through the 1st POD in group 1 and through the 3rd POD in group 2. These data demonstrate that the renal function of urine concentration is disturbed in the early phase following open-heart surgery even in the patients who have uneventful postoperative course.
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PMID:[Effects of open-heart surgery on renal function]. 279 87

The ability of the kidneys to excrete sodium and free water is often impaired in patients with cirrhosis. Sodium retention is a sine qua non for ascites formation. The impairment of water excretion causes hyponatremia and hypo-osmolality. In addition, these patients frequently have functional renal failure caused by intense renal vasoconstriction. The renin-angiotensin-aldosterone system and the sympathetic nervous system, which are activated in most cirrhotic patients with ascites, and a nonosmotic hypersecretion of antidiuretic hormone are important mechanisms of sodium and water retention. Angiotensin II and sympathetic nervous activity may also be involved in the pathogenesis of functional renal failure. The renal production of prostaglandins is increased in cirrhotic patients with ascites as a homeostatic response to antagonize the vascular effect of endogenous vasoconstrictors and the tubular action of antidiuretic hormone. Nonsteroidal anti-inflammatory drugs should, therefore, be administered with caution in these patients because they may induce acute renal failure and water retention. Although sulindac inhibits the renal synthesis of prostaglandins in cirrhotic patients with ascites, it appears to have less effect on renal function than do other nonsteroidal anti-inflammatory drugs administered to these patients.
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PMID:Renal function abnormalities, prostaglandins, and effects of nonsteroidal anti-inflammatory drugs in cirrhosis with ascites. An overview with emphasis on pathogenesis. 294 81

ANF is a newly discovered peptide hormone that has significant implications for critical care physicians. This hormone, released from the heart, is especially responsive to fluid challenges as well as to many of the drugs commonly used in the ICU, including pressor and anesthetic agents. It has potent arterial vasodilating effects in pharmacologic doses and may be an important natural vasodilating agent, especially in the renal vascular bed. In patients on dopamine, it may potentiate the renal vasodilating effect and may provide an effective therapy for developing acute renal failure. Children with congenital heart disease and patients with CHF have elevated levels that clearly alter the aldosterone-angiotensin II system and may help us to understand and treat these conditions more effectively. Additionally, ANF may be a marker for adequacy of treatment in these disease states. The potential uses for ANF include diuresis in patients with fluid overload and diuretic resistance, treatment of CHF, and as a short-acting vasodilator. In the ICU, many therapies affect cardiac pressures and volume regulation. Positive-pressure ventilation may decrease the release of ANF by decreasing venous return and thus contribute to water retention. Drugs used in the ICU may directly affect ANF levels and markedly affect the homeostasis of fluid and electrolyte balance. This hormone system interacts intimately with renin, angiotensin II, and aldosterone. These interactions may play a significant role in the development of essential hypertension. Although not addressed in this article, the treatment and understanding of essential hypertension may be significantly advanced by understanding these relationships. It is clear that ANF acts as a hormone with complex interactions between the heart, volume status, electrolyte balance, renin-angiotensin II-aldosterone, vasopressin, and vascular tone. Although currently no definitive picture exists for these complex interactions, this is an exciting new hormone with significant implications for patient management in the ICU. As research continues, the picture will become clearer and our understanding of this new hormone more precise.
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PMID:Atrial natriuretic factor in the pediatric intensive care unit. 297 48

All nonsteroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase, and consequently renal functions dependent upon prostaglandin synthesis can be affected. Fortunately, renal function in normal individuals is relatively independent of the PG system, and thus the NSAIDs don't usually produce any renal dysfunction. However, in some circumstances, inhibition of PG dependent renal functions can produce clinically significant effects. When the kidney is in a salt retaining state or when there is renal vascular damage, NSAIDs can reduce renal blood flow and glomerular filtration rate producing acute renal failure that is reversible upon discontinuation of the drug. NSAIDs can also: 1) reduce sodium excretion and blunt the diuretic effect of loop diuretics, thus producing or exacerbating edema, 2) inhibit PG dependent renin secretion occasionally resulting in hyperkalemia, 3) enhance the antidiuretic effects of vasopressin and 4) reduce the antihypertensive efficacy of several drugs. Evidence that any NSAID "spares" renal cyclooxygenase is controversial, and no NSAID is devoid of clinical problems. Syndromes that are less obviously related to inhibition of renal PG synthesis are acute interstitial nephritis with or without the nephrotic syndrome, renal papillary necrosis, and chronic interstitial nephritis. Recently a unique syndrome of flank pain and mild reversible renal dysfunction has been described in healthy individuals receiving suprofen, a uricosuric NSAID. This syndrome may be due to uric acid crystal deposition in the renal tubules and has resulted in the removal of suprofen from the US market.
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PMID:Renal effects of nonsteroidal anti-inflammatory drugs. 314 36

This chapter reviews the disturbances of the serum sodium and potassium concentrations, acid-base imbalances, and acute renal dysfunction that are seen frequently in alcoholic patients. The hyponatremia common in decompensated cirrhotics is caused by an impairment of renal free water clearance and concomitant water ingestion. Excessive proximal renal tubular sodium reabsorption and nonosmotic vasopressin release underlie the defect in renal water excretion in cirrhosis. Restriction of water intake is the principal therapeutic measure for hyponatremia. Hypokalemia is common in alcoholics but when observed does not always represent true potassium depletion. Although most cirrhotics have a diminished total body potassium content, intracellular potassium concentration is usually normal. In some patients gastrointestinal and renal potassium losses and nutritional potassium deficiency may cause true potassium depletion. Respiratory and metabolic alkalosis are the acid-base disturbances seen most frequently in alcoholics. Acidosis is relatively uncommon and is usually due to renal insufficiency, lactic acid or keto-acid accumulation. Toxin ingestion (methanol, ethylene glycol, or isopropanol) may also cause severe acidosis. Rhabdomyolysis, common in severe alcoholism, may produce various electrolyte disturbances and acute renal failure. The prognosis for recovery is good although temporary dialysis may be necessary.
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PMID:Disorders of the serum electrolytes, acid-base balance, and renal function in alcoholism. 370 21


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