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)

Although acute renal failure, caused either by renal ischemia or nephrotoxic agents, is usually characterized by oliguria, a severe fall in glomerular filtration rate, and a fall in renal blood flow, some patients and experimental models display a non-oliguric pattern of renal injury. The present study was designed to evaluate the mechanism of preservation of high urinary flow rate under this condition. Following the administration of the aminoglycoside gentamicin to rats for five days, a decrease in concentrating ability was demonstrated, caused by impaired vasopressin-mediated water transport. Further treatment resulted in a fall in Cin to 15 percent of control, although RBF was reduced to only 67 percent of control, and urine flow rate rose above control levels. Induction of acute and renal failure with dichromate was associated with variable high or low urinary flow rates according to pre-injury intake of sodium. Urine volume correlated directly with cortical blood flow. These data suggest that the non-oliguric pattern of acute renal injury is caused by preservation of cortical perfusion in the setting of severe tubular injury.
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PMID:Studies on the mechanism of non-oliguric experimental acute renal failure. 732 6

Acute renal failure was produced in vasopression-pretreated rabbits by clamping the left renal pedicle for one hour and removing the opposite kidney. Treatment with clonidine, as antihypertensive drug that blunts the kidney's response to vasopressin, resulted in significantly higher creatinine clearance and urine flow rate in the first 6 hours after unclamping. Clonidine (30 microgram/kg given intravenously 30 minutes before unclamping) also significantly lessened the number of hyaline casts in outer medullary tubules and inner medullary loops of Henle 6 hours after unclamping and reduced the number of abnormal tubular contours in microadiograms produced by infusing barium sulfate into the renal artery at sufficient pressure to rupture glomerular capillaries, causing an escape of contrast material into the tubules. The spaces consistently observed between the ends of barium columns and hyaline casts in microdissection studies and the great lengths of the hyaline casts suggest that hyaline casts obstruct the flow of tubular fluid. Clonidine treatment resulted in fewer, shorter, and thinner hyaline casts. These results indicate that tubular obstruction by hyaline casts plays an important role in early postischemic acute renal failure, and that clonidine's beneficial effect is due in part to a reduction in cast formation.
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PMID:The effect of clonidine on tubular obstruction in postischemic acute renal failure in the rabbit demonstrated by microradiography and microdissection. 735 Aug 13

Renal artery occlusion has been extensively used in animal models to cause acute renal failure. The present isolated tubule microperfusion studies were designed to examine the transport characteristics of multiple nephron segments of the rabbit after 60 min of total renal ischemia. Preliminary studies showed that this maneuver produced significant and persistent elevations of serum creatinine. The tubules were perfused and bathed with artificial solutions simulating ultrafiltrate and studied at 37 degrees C. Four nephron segments were examined. Ischemia reduced proximal convoluted tubule fluid reabsorption 77% (0.72 +/- 0.11 vs. 0.14 +/- 0.06 nl . mm-1 . min-1, P less than 0.01) and cortical proximal straight tubule fluid reabsorption 88% (0.54 +/- 0.10 vs. 0.06 +/- 0.03 nl . mm-1 . min-1, P less than 0.005). Ischemia reduced the ability of the thick ascending limb of Henle's loop to lower perfusate chloride ion concentration 60% (-47 +/- 9 vs. -19 +/- 3 meq/liter, P less than 0.02) and its diluting ability 49% (-87 +/- 15 vs. -44 +/- 7 mosmol/kg H2O, P less than 0.01). Ischemia reduced the antidiuretic hormone-dependent osmotic water permeability of the cortical collecting tubule 59% (0.0203 +/- vs. 0.0083 +/- 0.0020 cm/s, P less than 0.01). Morphologic alterations were noted in the proximal segments but not in the distal segments of the nephron. The current studies demonstrate that 60 min of renal ischemia impairs the transport capability of all proximal and distal nephron segments studied.
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PMID:Isolated nephron segments in a rabbit model of ischemic acute renal failure. 739 91

Clonidine, an antihypertensive drug that inhibits renin release and causes a water diuresis in normal animals, was tested for its ability to reduce the severity of post-ischemic acute renal failure produced in rabbits by clamping the left renal pedicle for 1 hour and removing the opposite kidney. Clonidine significantly lessened renal failure when given during, or 1 hours after, the ischemic insult in dehydrated rabbits. It was also effective when given during the ischemic insult in vasopressin-treated water-drinking rabbits but not in control water-drinking rabbits. In vasopressin-treated rabbits, clonidine lessened renal failure observed 2 days after the ischemic insult despite the fact that in the immediate postischemic period it lowered total renal blood flow, produced hypotension, and did not bring about lower plasma renin levels. Clonidine treatment resulted in less outer medullary microvascular damage (demonstrated by colloidal carbon staining), higher outer medullary blood flow 1 to 2 hours after unclamping, fewer casts, and higher creatinine clearance and free water clearance/creatinine clearance 4 to 6 hours after unclamping compared with controls. The effect of clonidine was unrelated to plasma renin activity. Clonidine did not alter plasma vasopressin concentration. Demeclocycline and lithium, two agents that blunt renal responsiveness to vasopressin, had a beneficial effect in dehydrated animals similar to that of clonidine, but the angiotensin II antagonist saralasin and the angiotensin converting enzyme inhibitor SQ20881 did not. Normal rabbits given a large dose of vasopressin in oil plus clonidine had significantly greater urine output and free water clearance and lower urine osmolality than did rabbits given vasopressin in oil alone. These results suggest that clonidine may be beneficial because it prevents ischemic microvascular injury in the renal outer medulla, an effect that may decrease tubular obstruction by lessening desquamation of damaged tubular cells or cell constituents into the tubular lumen. Clonidine may also decrease formation of obstructive hyaline casts in collecting ducts by blunting the kidney's response to vasopressin and increasing tubular fluid flow rate.
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PMID:Clonidine after renal ischemia to lessen acute renal failure and microvascular damage. 746 46

Diagnostic and therapeutic angiography has demonstrated an important role in gastrointestinal hemorrhage. During the past 2 years, we performed angiography in the management of 20 patients with uncontrolled gastrointestinal bleeding. Conservative management including medication and transfusion would not appear to suffice in these patients and most patients had been evaluated to have a high operative risk in our series. Ten of the 20 patients had renal dysfunction (creatinine > 1.7 mg/dl) before angiography. The role of angiography in the management of patients with renal dysfunction remains controversial because angiography is likely to produce acute renal failure. We performed angiography to stop bleeding in these patients with renal dysfunction because they could die of blood loss. In our 20 cases, bleeding sites were identified in 14 patients. The detection rate was 70%. Thirteen of the 14 with the use of either vasopressin infusion or arterial embolization showed complete cessation of bleeding in 10 patients. Three cases failed to be controlled. One received an operation after a bleeding site was located by angiography. In our study, sepsis with renal failure was the leading cause of mortality (6 cases). Ten patients with pre-existing renal dysfunction had angiography performed and only one showed abrupt elevation of creatinine levels after angiography. He also developed sepsis. Deterioration of renal function was possibly due to angiography or more likely due to sepsis and hypovolemia. Six patients died of sepsis after angiography although 4 of these patients showed cessation of bleeding. Four cases with pre-existing renal dysfunction and without evidence of infection survived after angiographic management.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Angiography for the management of poorly controlled gastrointestinal hemorrhage--20 cases clinical observation]. 770 50

Continuous pump-driven veno-venous hemofiltration (CVVH) has become an established method for treatment of acute renal failure (ARF). Since severe disturbances of (micro-) circulation are intimately involved in the bad outcome of these patients, the profile of endocrinological regulators of circulation was prospectively and serially measured in patients undergoing pump-driven CVVH (n = 15). 15 patients with similar APACHE II score, but without ARF and without CVVH were also studied. Endothelin-1 (ET-1), atrial natriuretic peptide (ANP), vasopressin, renin, and catecholamine (epinephrine, norepinephrine) plasma levels were measured before start of CVVH (= "baseline") (in the non-CVVH patients: admission to intensive care unit) and during the next 5 days. Various hemodynamic parameters were additionally monitored. MAP, HR, PAP, CI, and right ventricular hemodynamics (RVEF, RVEDV, RVESV) remained almost unchanged in the CVVH patients and were without differences to the non-CVVH group within the entire investigation period. PCWP and RAP were higher in the CVVH patients already at baseline (RAP, 17.8 +/- 4.0 mmHg; PCWP, 22.1 +/- 4.5 mmHg) (p < .02) and remained elevated in the further course of the investigation. Renin plasma level was higher already at baseline in the CVVH patients (907 +/- 184 pg/ml) (p < .05) and further increased during CVVH (to 1453 +/- 186 pg/mL). Vasopressin increased only in the CVVH group (from 3.80 +/- .66 to 11.85 +/- 1.05 pg/mL) (p < .01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Changes in regulators of circulation in patients undergoing continuous pump-driven veno-venous hemofiltration. 2597 10

Xanthopterin (XPT), an unconjugated pteridine compound, affects cell growth and differentiation. When injected into rats, XPT has caused changes that have been interpreted as renal growth and hypertrophy. In the present study, we investigated the effect of intraperitoneal administration of XPT on the renal function in the rat. XPT administration was associated with polyuria and a reversible form of nonoliguric acute renal failure (ARF), with renal function declining maximally after 2 days and returning to normal after 7 days. The polyuria was due, at least in part, to a concentrating defect that was vasopressin resistant. The ability of XPT to induce ARF was modulated by dietary salt intake, being enhanced by a low-sodium diet and prevented by a high sodium intake. Histological examination of the kidneys showed intratubular crystal deposition and acute tubule necrosis, suggesting that XPT induces crystal nephropathy. There was an increase in wet and dry weights of the kidney and an increased DNA/protein ratio, compatible with a hyperplastic response. Because the severity of other crystal nephropathies may be modulated by urine flow rate and pH, we studied the ability of water diuresis or alkaline diuresis to protect against XPT-induced ARF. Both water diuresis and HCO3 loading blunted the ability of XPT to decrease renal function. The change in renal function induced by XPT in the various groups was paralleled by corresponding changes in the levels of XPT-like substances in the kidney and by the amount of crystal deposition. Thus, XPT injection induces crystal nephropathy, the severity of which can be modulated by dietary salt intake, urine pH, and urine flow rate.
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PMID:Xanthopterin-induced renal dysfunction: a reversible model of crystal nephropathy. 789 1

Cisplatin is an antineoplastic agent. Several nephrotoxic effects are associated with its use including chronic and acute renal failure, renal magnesium wasting, and polyuria. We have investigated polyuria in groups of rats treated with cisplatin at doses of 2.5 and 5 mg/kg body weight given once weekly for 3 weeks to determine possible mechanisms of this impairment. After cisplatin administration, glomerular filtration rate was reduced and significant increases in sodium and water loss were also seen. These changes were associated with decreases in urinary cAMP. Inner medullary collecting duct (IMCD) cells were removed from these animals and were stimulated with graded doses of vasopressin. Cells from cisplatin-treated rats showed an impaired response in cAMP generation to vasopressin stimulation as compared to cells from normal animals. To determine more precisely the site of impairment, the adenylate cyclase complex of the IMCD cells was further studied with forskolin and NaF. Forskolin was used to probe the catalytic unit activating adenylate cyclase, and NaF the guanine nucleotide regulatory protein (G protein). In response to forskolin, cells from cisplatin-treated rats and normal rats responded similarly in generating cAMP. However, following NaF, the cAMP response was blunted in the cells from the cisplatin rats. These results suggested that the catalytic unit was not injured by cisplatin (forskolin study) but the G protein was (NaF). In conclusion, the present study suggests that the polyuria seen following cisplatin administration is associated with an end-organ resistance to vasopressin manifested by reduced cAMP generation, secondary in part or whole to a defect at the level of the G protein.
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PMID:Mechanism of polyuria after cisplatin therapy. 830 21

Water loading only rarely results in adverse effects due to the high efficiency of the kidney in excreting free water. However, when renal diluting ability is impaired, such as in inappropriate vasopressin secretion, water intoxication can occur in otherwise normal individuals. We report the case of a 19-year-old man with acute voluntary water intoxication following exercise, which resulted in a transient defect in renal diluting capability. Hyponatremia was further complicated by rhabdomyolysis. We review the literature regarding other cases of hyponatremia following excessive water intake, and discuss the possible association between hyponatremia and rhabdomyolysis. We conclude that monitoring of muscle enzymes is indicated in acute hyponatremia, to allow for timely intervention intended to prevent rhabdomyolysis-associated acute renal failure.
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PMID:Transient exercise-induced water intoxication and rhabdomyolysis. 843 Jun 83

Therapy with foscarnet is associated with acute renal failure. Prior studies have emphasized foscarnet's proximal tubular toxicity, but there have been isolated reports of foscarnet-induced nephrogenic diabetes insipidus. As a phosphate analog, foscarnet is a competitive inhibitor of NaPO4 cotransport. However, foscarnet's effect on antidiuretic hormone (ADH)-induced transport has not been previously investigated. We studied foscarnet's modulation of transport in the toad urinary bladder. Foscarnet at 10 microM to 10 mM did not alter basal water or urea flux. Urea transport induced by a maximal dose of ADH (24 mIU/ml) was inhibited by 0.1 to 5.0 mM foscarnet. In tissues challenged with 0.5 to 1.0 mIU of ADH per ml, 1.0 to 10 mM foscarnet increased water flow but did not alter urea flux. Foscarnet also increased water flow induced by 1.0 to 10 microM forskolin. In tissues pretreated with 10 microM naproxen, foscarnet did not alter water flow induced by 0.5 to 1.0 mIU of ADH per ml or forskolin. These results indicate that foscarnet stimulates water flow induced by 0.5 to 1.0 mIU of ADH per ml at a site proximal to that of the generation of cyclic AMP and inhibits urea flux induced by a maximal dose of ADH at a separate site. In humans, foscarnet nephrotoxicity is likely not limited to the proximal nephron, but extends to the collecting duct. Patients receiving foscarnet should be closely monitored for disorders of urinary concentration.
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PMID:Foscarnet alters antidiuretic hormone-mediated transport. 854 Jul 7


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