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)

Hypouricemia seen with hyponatremia related to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) results from an increase in uric acid renal clearance. We studied the mechanism of the increase of uric acid excretion in 6 SIADH patients through pyrazinamide (PZA), which decreases tubular secretion of uric acid, and sulfinpyrazone (SPZ) which decreases post-secretory reabsorption of uric acid. 3 g of PZA decreased the absolute uric acid excretion from 428 +/- 244 to 105 +/- 47 micrograms/min (mean +/- SD, p less than 0.01), and 300 mg of SPZ increased the uric acid to creatinine clearance ratio from 0.31 +/- 0.05 to 0.52 +/- 0.05 mg/dl glomerular filtration rate (mean +/- SEM, p less than 0.001), which represent an increment about half of that observed in the control group. The increase of uric acid clearance in SIADH seems to result from a decrease in the post-secretory reabsorption of uric acid. After SPZ, we saw a decrease of natriuresis from 5.6 +/- 1.4 to 1.8 +/- 0.3 mmol/h (p less than 0.001), without any change of urinary flow or urinary potassium excretion.
Nephron 1985
PMID:Mechanisms of hypouricemia in the syndrome of inappropriate secretion of antidiuretic hormone. 397 80

To further evaluate the interaction between vasopressin (AVP) and prostaglandin E2 (PGE2) in the kidney, the effects of AVP and PGE2 on cell cAMP content were examined in the isolated thick ascending limb of Henle (TAL) and the cortical collecting tubule (CCT) of rat kidney. Nephron segments were incubated in the presence of phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine (MIX), with 10 nM AVP and varying concentrations of PGE2 at 37 degrees C for 1-7 min, and the cAMP content was determined by radioimmunoassay. PGE2 suppressed the AVP-stimulated increase in cell cAMP in both medullary (MTAL) and cortical (CTAL) portions of the TAL in a dose-dependent manner. This inhibitory effect was evident at 0.28 nM PGE2 and maximum at 2.8-28 microM PGE2. By contrast, in the presence of MIX PGE2 did not inhibit AVP-stimulated cAMP increases in the CCT. However, in the absence of MIX, PGE2 suppressed cAMP accumulation in the CCT. These data suggest that PGE2 may suppress cell cAMP by inhibiting AVP-dependent cAMP formation in the TAL; PGE2 may suppress cAMP in the CCT by acting at a site(s) affected by MIX and not by inhibiting cAMP formation. The results show that although PGE2 may inhibit AVP-dependent cell cAMP accumulation in both TAL and CCT, the underlying cellular mechanisms may be different in these two distinct AVP-sensitive nephron segments.
 ...
PMID:Effect of PGE2 on vasopressin-dependent cell cAMP in isolated single nephron segments. 619 77

Light and electron microscopy were used to study the effects of a lithium-supplemented diet on renal structure in the rat. At the end of a 7-week experimental period serum lithium levels were 1.14 +/- 0.20 mM. Lesions consisting of groups of dilated tubules were found in the immediate vicinity of the interlobular arteries in all experimental animals. These tubules were identified as the connecting tubule or the initial portion of the collecting tubule. The epithelium of these tubules was generally flattened but was punctuated by markedly swollen epithelial cells. PAS-positive deposits found in both types of cells were identified as glycogen. Electron microscopy revealed considerable lithium-induced damage in the swollen cells including increased numbers of mitochondria, many of which were swollen or otherwise damaged, dilated cisternae of endoplasmic reticulum and vacuolization of the apical cytoplasm. The flattened cells of these tubules were similar to the dark or intercalated cells of normal collecting tubules. Some detachment of epithelial cells from their basement membrane was evident in these tubules. Damage was less severe in distal convoluted tubules. Lithium-induced changes were not observed in glomeruli, proximal tubules or ascending thick limbs of Henle. In medullary collecting tubules damage was less severe than in cortical collecting tubules, but detachment of epithelial cells was a common finding. The interstitial tissue of the papilla exhibited histochemical and ultrastructural changes consistent with lithium blockade of the action of antidiuretic hormone. The ultrastructural damage to cortical tubules is similar to that found in patients receiving therapeutic lithium for long periods of time. The anatomic sites of lithium-induced pathology correspond to the location of lithium-induced pathophysiology.
Nephron 1983
PMID:Effects of lithium on the structure of the rat kidney. 686 74

Plasma arginine-vasopressin (AVP) was measured before and after 24 h of a 26-hour renal concentration test in 47 patients treated with lithium for 6-180 months (mean 70 months). In 34 of the patients, plasma AVP was also measured before and after a 2- to 4-hour period of water loading, and in 31 of the patients, creatinine, 125iothalamate, 131I-hippuran and lithium clearances were measured. Plasma AVP values were compared to those obtained in 8 healthy controls. Baseline AVP levels were significantly higher in the lithium-treated patients than in healthy controls. During the period of water deprivation AVP values increased significantly and during oral water loading a significant decrease took place, AVP values still being significantly higher in the lithium-treated patients than in the healthy controls. During oral water loading a slight increase in lithium clearance as well as fractional lithium excretion was seen as compared to values obtained during the last 2 h of a renal concentration test. This study demonstrates that antidiuretic hormone production is neither blocked nor inhibited during lithium treatment. The hypothalamic system reacts on water deprivation as well as on water loading. This study supports the notion that the main lithium-induced renal affection is a vasopressin-resistant impairment of renal concentrating ability.
Nephron 1982
PMID:Plasma arginine-vasopressin, renal-concentrating ability and lithium excretion in a group of patients on long-term lithium treatment. 717 89

Micropuncture and clearance studies were performed on normal untreated and polyuric lithium chloride treated rats (10-12 days). A persistent hypernatremic state quickly developed in the polyuric lithium treated rats during hydropenia resulting from an increased urinary loss of water over sodium chloride, as the fractional excretion of sodium remained at control levels. Superficial proximal tubule and loop of Henle fluid reabsorption was depressed by 8 and 17%, respectively, in lithium-treated rats during this period. By contrast, water reabsorption in the distal tubule and collecting system was significantly increased in the lithium animals, being 27% of the filtered load compared with 20% in normal rats. These results suggest that the urinary-concentrating defect induced by lithium treatment is due primarily to a depression of proximal tubule and possibly loop of Henle function, and that water reabsorption within the distal nephron may in fact be augmented: thus it is unlikely that the action of antidiuretic hormone is significantly impaired. Marked phosphaturia and hypocalciuria were also noted in the lithium-treated rats.
Nephron 1980
PMID:Effect of lithium treatment on rat renal tubule function. Evidence against impaired antidiuretic hormone action. 739 71

The syndrome of inappropriate secretion of antidiuretic hormone is a common consequence of neurologic and pulmonary infections as well as drug intake and many other clinical situations. Its association with herpes varicella-zoster virus infections is scarcely reported in the literature. It generally appears in immunosuppressed patients suffering from serious underlying diseases. There are also a few cases of syndrome of inappropriate secretion of antidiuretic hormone related to vidarabine use. We report the case of a man infected by human immunodeficiency virus who developed a disseminated herpes varicella-zoster virus infection and symptoms due to hyponatremia caused by antidiuretic hormone excess. The patient was cured with saline hypertonic infusion, water restriction, and intravenous administration of acyclovir. To the best of our knowledge, this is the first case of this association in a human immunodeficiency virus infected patient. We propose the use of acyclovir instead of vidarabine in the management of these situations.
Nephron 1994
PMID:Syndrome of inappropriate antidiuretic hormone secretion and herpes zoster infection: 1. Report of this association in a patient suffering from AIDS. 783 Aug 68

The effects of hormone stimulation on atrial natriuretic factor (ANF) release in atria were studied in experimental renal failure rats. In vitro experiments were done in two groups of male Wistar rats. Group 1 rats were sham operated, and group 2 rats were subjected to 5/6 nephrectomy. Overall glomerular filtration rate was significantly reduced (1.98 +/- 0.10 vs. 0.75 +/- 0.05 ml/min, p < 0.001) in nephrectomized rats. These rats were also mildly uremic [blood urea nitrogen (BUN): 18 +/- 0.6 vs. 60 +/- 3.9 mg/dl p < 0.001]. The right atria of partially nephrectomized and sham-operated rats were isolated and perfused in a modified Langendorff apparatus to measure ANF release rate. Experiments were done in two phases. In the initial phase, spontaneous release of ANF was measured. In the second phase, angiotensin II (10(-6) M), vasopressin (10(-6) M) or endothelin (ET 1; 10(-6) M) were added into the perfusate. Spontaneous ANF release by the atria of renal failure rats was significantly elevated compared to intact rats. A significant positive correlation was found between ANF release rate and BUN (r = 0.65, p < 0.01). This suggests that the increase in ANF release by the atria of chronic renal failure (CRF) rats is related to the severity of renal impairment. Angiotensin II, vasopressin and endothelin induced exaggerated increases in ANF release by the atria of CRF rats. These results show that a shift in stimulus response curve is present and can contribute to the observed increase in plasma ANF levels in CRF rats.
Nephron 1995
PMID:In vitro hormone-stimulated atrial natriuretic factor release is increased in experimental renal failure. 789 99

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.
Nephron 1995
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.
Nephron 1993
PMID:Mechanism of polyuria after cisplatin therapy. 830 21

The mechanisms responsible for the increased renal clearance of uric acid in the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) are not fully clarified. Studies using either pyrazinamide or probenecid, or both drugs but at an interval of several days, could not undoubtedly distinguish the 'hypersecretory theory' from the one favoring a defect in either post- or presecretory reabsorption. We decided to do a combined pyrazinamide and probenecid test in 5 patients with hyponatremia due to SIADH in order to evaluate more clearly the respective importance of these different pathways. Our results allow the conclusion of a diminished presecretory and mainly postsecretory reabsorption (80 +/- 4.6 and 14 +/- 3% of filtered load, respectively). As far as the secretion of uric acid is concerned (17 +/- 10% of filtered load), we may say that this pathway is adapted to the amount of hypouricemia.
Nephron 1993
PMID:Evidence of defective tubular reabsorption and normal secretion of uric acid in the syndrome of inappropriate secretion of antidiuretic hormone. 832 49


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