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)

Evidence that an increase in plasma atrial natriuretic peptide (ANP) concentrations mediates, at least in part, glomerular hyperfiltration in diabetic rats prompted us to study the relationship between ANP and renal haemodynamics in hyperfiltering type 2 diabetic patients in association with other hormones implicated in the control of glomerular filtration rate (GFR) (catecholamines, vasopressin, renin) and in sodium tubular transport (aldosterone, ouabain-displacing factor, ODF). Since hyperglycaemia is also associated to hyperfiltration, diabetic patients who presented with secondary drug failure were studied both in hyperglycaemic and in normoglycaemic condition. For this purpose, 11 normotensive non-macroproteinuric hyperfiltering patients with type 2 diabetes were treated with an 8-day continuous insulin infusion (days 0-7). Dehydration was prevented or corrected and natriuresis was on day 0 above 100 mmol/day. The following parameters were determined on days 0 and 7: GFR and renal plasma flow (RPF) by 99mTc-DTPA and 131I-hippuran clearances; the extracellular volume, assimilated to the DTPA diffusion volume; urinary ODF by receptor-binding assay and urinary as well as plasma catecholamines by HPLC after extraction on alumin. Plasma ANP and antidiuretic hormone (ADH) were measured by radioimmunoassay after extraction on phenyl-silylsilica (ANP) and with ether (ADH). Unextracted plasma was used for radioimmunological measurement of plasma renin activity and aldosterone. When correcting hyperglycaemia to normoglycaemia GFR decreased from high to normal mean value (138 +/- 27 and 115 +/- 6 ml/min, p < 0.001), RPF followed the same trend, and the DTPA diffusion volume did not change.(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1993
PMID:Natriuretic and vasoactive hormones and glomerular hyperfiltration in hyperglycaemic type 2 diabetic patients: effect of insulin treatment. 844 67

We report a case of phosphate diabetes in a patient with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH) associated with sarcoidosis. Our patient was affected by systemic sarcoidosis and he fits the criteria of Schwartz for the diagnosis of SIADH. He presented with phosphate diabetes which appeared during demeclocycline (DMC) therapy and persisted for about 1 month from the end of DMC. It constitutes the fourth case of phosphate diabetes induced by tetracycline described in the literature and it is the third case of SIADH associated with sarcoidosis.
Nephron 1993
PMID:Demeclocycline-induced phosphate diabetes in a patient with inappropriate ADH secretion and systemic sarcoidosis. 845 Sep 17

Our purpose was to compare the effect of urea and indomethacin on solute excretion in hyponatremic patients with inappropriate secretion of antidiuretic hormone (SIADH). In 6 patients (serum Na: 126 +/- 3 mmol/l), the intake of urea (0.1 g/kg) induced a decrease in sodium excretion while urine osmolality, urine flow and osmotic clearance (Cosm) did not change. In the control group, the urinary flow and Cosm were increased as expected, while sodium excretion tended to increase. In the SIADH group, the decrease in the fractional excretion (FE) of Na+ (FE.Na+) (or FE.Cl-) after urea intake was negatively correlated with urinary urea concentration while the FE.K+ was positively correlated with FE.Na+ (or FE.Cl-), which suggests that the effect of urea on sodium excretion takes place proximally to the distal tubule, probably at the thin ascending limb. After indomethacin intake, FE.Na+ (or FE.Cl-), FE.K+, Fe.osm and Fe.urea decreased in the normal and hyponatremic groups. The mean free water reabsorption relatively to osmolar delivery was lower in SIADH (p < 0.05), and did not change significantly after indomethacin intake. The fact that the decrease of FE.Na+ (or FE.Cl-) after indomethacin was associated with a decrease in FE.K+ suggests that the increase in sodium (or chloride) reabsorption occurred more proximally to the distal tubule (probably a the medullary segment of the thick ascending limb of the loop of Henle).
Nephron 1993
PMID:Effect of urea and indomethacin intake on solute excretion in the syndrome of inappropriate secretion of antidiuretic hormone. 850 36

To understand the regulation of vasopressin receptors in an animal model of hypertension, localization and age-related changes in renal arginine vasopressin (AVP) receptors in spontaneously hypertensive rats (SHR) were investigated using in vitro (macro) autoradiography and a radiolabeled receptor assay. Autoradiography localized renal AVP V2 receptors to the distal tubules and collecting ducts in the medulla. We also found small numbers of AVP-binding sites within glomeruli, possibly representing V1 receptors in the mesangium. The radiolabeled receptor assay of the medulla membrane fraction revealed that the binding affinity of renal V2 receptors did not differ significantly between SHR and control Wistar-Kyoto rats in any age group. However, the binding capacity (Bmax) for V2 receptors in 12-week-old SHR was significantly increased (p < 0.025) as compared with that of age-matched control rats. The Bmax values for V2 receptors in 3- and 7-week-old SHR were not significantly different from those of age-matched controls. There was no significant change in urine volume between SHR and control rats at the age of 12 weeks. The mean plasma AVP concentration in SHR increased at 7 and 12 weeks of age. These findings suggest that SHR have different developmental changes in kidney AVP receptors and that renal V2 receptors play a role in maintaining fluid homeostasis in SHR with established hypertension.
Nephron 1996
PMID:Autoradiographic localization and age-related changes in vasopressin receptors in spontaneously hypertensive rats. 868 40

1. Renal tubules and, in particular, the inner medullary collecting duct, produce endothelin and express cognate receptors. 2. Endothelins inhibit vasopressin-stimulated cAMP accumulation and water reabsorption in the collecting duct; endothelins may also inhibit sodium reabsorption in the proximal tubule and collecting duct. 3. Autocrine inhibition of sodium and water reabsorption in the inner medullary collecting duct by endothelin may play a role in maintaining extracellular fluid volume homeostasis. 4. Derangements in autocrine inhibition of sodium and water reabsorption in the inner medullary collecting duct by endothelin may be involved in the pathogenesis of the hypertensive state. 5. Nephron-derived endothelins may function in a paracrine manner to regulate interstitial, juxtaglomerular and vascular smooth muscle cell function.
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PMID:Endothelins: renal tubule synthesis and actions. 871 71

Urea absorption in the inner medullary collecting duct provides a mechanism to elevate the concentration of urea in the papillary interstitial fluid and thereby permit the excretion of urea with as little water as possible. Urea reabsorption may have another important effect - to aid in the excretion of potassium (K). K excretion depends on two processes: first, factors such as aldosterone which cause the concentration of K in the luminal fluid of the cortical distal nephron to be high and, second, factors which augment the flow rate through those nephron segments. Since, the osmolality of the luminal fluid in the cortical collecting duct (CCD) and plasma are equal when antidiuretic hormone acts, the flow rate in the CCD is dependent on solute delivery. Urea is a major solute in the lumen of the CCD and thereby plays an important role in maintaining the CCD flow rate. Since urea and K are often found in the same foods, having urea help the excretion of K is potentially advantageous. If the excretion of urea was low, the flow rate in the terminal CCD would decline. In this circumstance, the luminal K concentration would have to rise in proportion to the fall in flow rate or there would be a diminished rate of excretion of K and, possibly, hyperkalemia.
Nephron 1996
PMID:Urea recycling: an aid to the excretion of potassium during antidiuresis. 873 Apr 12

Three patients with autosomal-recessive nephrogenic diabetes insipidus (NDI), homozygous for mutations in the aquaporin 2 gene (AQP2), were tested for their fibrinolytic and hemodynamic responses to intravenous administration of 1-desamino-8-D-arginine vasopressin (DDAVP). They all showed an increase of tissue-type plasminogen activator antigen, facial flushing, an increase of heart rate and a decrease of diastolic blood pressure. These results confirm the hypothesis that NDI patients with an AQP2 defect can be discriminated from NDI patients with a vasopressin type 2 receptor defect by their normal extrarenal responses to DDAVP.
Nephron 1996
PMID:Normal fibrinolytic responses to 1-desamino-8-D-arginine vasopressin in patients with nephrogenic diabetes insipidus caused by mutations in the aquaporin 2 gene. 873 Apr 18

The effect of orally available, nonpeptide vasopressin V1 and V2 receptor antagonists on chronic progressive glomerular disease was investigated in Wistar rats with Adriamycin-induced nephropathy. At weeks 0 and 3, Adriamycin was injected twice, and at week 3 drugs started to be given as follows: groups 2 and 3 were treated with V1 and V2 antagonists, respectively, while the untreated group 1 served as control. To block the effects of vasopressin totally, both V1 and V2 antagonists were simultaneously administered (group 4). At weeks 8 and 10, V1 and V2 antagonists given either alone or combined significantly reduced the urinary protein excretion to the same levels. Urinary volume increased in groups 3 and 4 from week 4. Systolic blood pressure did not significantly increase in all groups during the study. Histological alterations in the kidney of groups 2, 3 and 4 were significantly attenuated compared to the control. These results suggest that both vasopressin V1 and V2 agonism plays a role in the pathophysiology of Adriamycin-induced nephropathy despite plasma levels of vasopressin within the normal range. These findings also lead to the notion that in some types of nephrotic patients these orally available V1 and/or V2 receptor antagonists may be effective for reduction of proteinuria and for retardation of progression of renal failure.
Nephron 1996
PMID:Evidence for the involvement of vasopressin in the pathophysiology of adriamycin-induced nephropathy in rats. 873 Apr 39

The effects of the nonpeptide orally effective vasopressin V1 receptor antagonist OPC-21268 were studied in progressive focal glomerulosclerosis (FGS) which developed in spontaneously hypercholesterolemic (SHC) rats with manifestations of hypercholesterolemia and proteinuria. Unilateral nephrectomy was performed at 7 weeks of age to accelerate spontaneous FGS. After nephrectomy, OPC-administered rats were fed chow containing 1% OPC-21268 for 9 weeks. Treatment with vasopressin V1 antagonist significantly reduced the rate of increase in the levels of triglyceride, systolic blood pressure, serum creatinine and BUN, and prevented a significant deterioration in creatinine clearance. Rats were sacrificed at 16 weeks of age. Histologically, the index of glomerular sclerosis in the OPC group showed a significant decrease compared to that in the control group (2.2 +/- 0.1 vs. 2.6 +/- 0.1, p < 0.01). Relative interstitial volume and glomerular volume in the OPC group showed a tendency to decrease compared to those in the control group. These results indicate that vasopressin plays an important role through V1 receptors in the development of glomerulosclerosis, and vasopressin V1 antagonist may prevent the progression of renal injury in glomerulosclerosis.
Nephron 1996
PMID:Effect of a nonpeptide vasopressin V1 antagonist (OPC-21268) on experimental accelerated focal glomerulosclerosis. 885 62

Hypotension is frequently encountered during hemodialysis (HD). One of the main factors of the HD-induced hypotension is acute reduction of circulating plasma volume by water removal, which is induced by the poor plasma refilling from the extravascular space into vessels. The determinants of plasma refilling, however, have not been clearly identified. Recently, we devised a mathematical model of water transport in HD patients, which can estimate the plasma-refilling coefficient (Kr) during HD. In the present study, we evaluated the factors determining plasma refilling by using this model. In 13 patients undergoing regular HD, the changes of Kr during HD were calculated from the model. Levels of ANP, cGMP, cAMP, endothelin, angiotensin II and vasopressin were measured before and after HD. Kr fell from 750.4 +/- 558.0 to 112.8 +/- 81.9 ml/mm Hg/h during HD. The rate of water removal during HD showed no significant correlation with the changes of Kr. Among the hormones and nucleotides measured here, plasma ANP level and cGMP were significantly correlated with Kr (r = 0.78, p < 001 and r = 0.62, p < 0.01, respectively). Our findings suggest that severe reduction in the level of serum ANP during HD, which is induced by water removal, plays some role in HD-induced hypotension through the attenuation of plasma refilling in HD patients.
Nephron 1996
PMID:A study on regulating factors of plasma refilling during hemodialysis. 888 15


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