Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diffusional and osmotic water permeability of collecting ducts in isolated papillae of rats' kidneys were measured in papillae taken from normal and lithium pretreated rats. The diffusional water permeability of collecting ducts in papillae from normal rats in the absence of ADH was 4.1 +/- 0.2 (S.E.M.) (n = 18) muM s-1 increasing to 7.2 +/- 0.6 mum s-1 with ADH. Values obtained with lithium (10 mM) in the medium, perfusate or both and in papillae taken from lithium pretreated rats did not differ significantly from the above. The cyclic AMP content of the papillae taken from normal rats was 83 +/- 6 pm mg protein in the absence of ADH and increased to 196 +/- 12 (n = 13) with 500 mu units ml-1 ADH. Lithium 10 mM in the medium did not alter this response. Papillae from lithium pretreated rats had a similar basal level of cyclic AMP but the increment in a lithium (10 mM) medium after ADH was significantly less. These results indicate that the impaired water handling of lithium treated rats is probably not due to a failure of the membrane to increase its permeability to water after ADH. Though lithium does alter the production of cyclic AMP this is not believed to be important regarding any alteration in water permeability. We believe it is probable that lithium interferes with sodium chloride transport at some more proximal nephron segment thereby producing the syndrome of polyuria.
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PMID:The effect of lithium on the permeability response induced in the collecting duct by antidiuretic hormone. 18 85

In baroreceptor denervated cats one internal carotid artery (ICA) or the cerebral ventricular system (CVS) was perfused with isotonic, hypertonic and hypotonic sodium chloride solutions. Renal sympathetic activity (RSA) and blood pressure (BP) were recorded. ICA perfusion with isotonic sodium chloride (150 mM NaCl) produced no changes of RSA compared to control level,. RSA was increased from plus 30% to plus 350% in 44 tests out of 45 tests following hypertonic (425 mM NaCl) ICA perfusion. RSA was decreased following hypotonic (aqua dest.) ICA perfusion from minus 30% to minus 100% in 37 tests out of 50 tests. The degree of RSA changes was found to depend upon the osmolarity of the solutions. 425mM NaCl and aqua dest. produced greater RSA changes than 290 mM NaCl and 75 mM NaCl. CVS perfusion with isotonic sodium chloride produced a slight increase of RSA compared to control levels (plus 15%). Hypertonic sodium chloride produced a RSA increase from plus 15% to plus 135% in 10 tests out of 14 tests. Hypotonic sodium chloride produced a RSA decrease from minus 15% to minus 80% in 8 tests out of 14 tests. Changes of RSA following ICA perfusions and CVS perfusions were accompanied by changes of BP in the same direction. A quantitative correlation between delta RSA and delta BP could not be found. Results suggest that renal osmoregulatory response to osmotic stimuli in the carotid artery may not just arise in response to changing ADH levels but may also be induced by changes in RSA.
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PMID:Influence of intracranial osmotic stimuli on renal nerve activity in anaesthetized cats. 116 65

Ten anephric patients were studied before and during hemodialysis. The extracorporeal circuit was primed with 5% albumin in 0.9% sodium chloride. Ultrafiltration volume removed by the hemodialyzer was replaced continuously. Modifications of a standard chronic renal failure dialysate were used to minimize changes in plasma urea while varying plasma sodium and calcium in opposite directions. Plasma ionized calcium concentrations in two patients confirmed other studies demonstrating a correlation between plasma total calcium and ionized calcium under these conditions. Plasma ADH determined by bioassay did not correlate with plasma osmolality, plasma sodium concentration, plasma potassium concentration, blood pressure, or pulse rate. The change in plasma ADH during dialysis was significantly correlated only with the change in plasma calcium (r = 0.47, p less than 0.05). The data support the hypothesis that plasma calcium plays a role in the regulation of ADH release in man, independent of the renin-aldosterone system.
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PMID:The effect of plasma calcium on plasma ADH levels in anephric patients. 126 17

Free water clearance (CH2O) was measured during hypotonic saline infusion in Sprague-Dawley and in Brattleboro (DI) rats with 131I-induced hypothyroidism and their age-matched controls. At peak urine flow, which was similar in hypothyroid DI (HDI) and control DI (CDI) rats, inulin clearance (CIn/kg) and CH2O/kg were 23 and 20% (P less than 0.02) lower in HDI. Fractional urine flow and fractional sodium excretion were 30 and 40% (P less than 0.001) higher in HDI. Utilization of distal delivery of filtrate for CH2O, formation was 16% less in HDI (P less than 0.01). Papillary osmolality was not higher in HDI rats. Data in Sprague-Dawley rats were similar to those of the DI rats, indicating that endogenous ADH was effectively suppressed. It is concluded: 1) delivery of filtrate out of the proximal tubule was not diminished in hypothyroid rats in spite of a decrease in CIn; 2) despite a similar delivery of filtrate to the distal diluting site, CH2O formation was less in hypothyroid rats than in controls; 3) these data suggest that a defect in the diluting segment could be unmasked at high rates of filtrate delivered to the distal nephron; 4) this defect could be either due to impaired sodium chloride reabsorption or due to increased backdiffusion of water in the distal nephron.
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PMID:Role of distal delivery of filtrate in impaired renal dilution of the hypothyroid rat. 126 72

Hyponatraemia (HN) can result from a wide range of mechanisms, and therapy must be individualized. Two theories of the origin of HN in acute brain disease have prevailed. The first is the cerebral salt wasting syndrome (CSWS), where excessive natriuresis caused by some unknown cerebral natriuretic factor lowers the total sodium pool of the body and hence the plasma concentration. The second theory is the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), where an increase in total body water is caused by unphysiological secretion of ADH, lowering the concentration of sodium in the plasma. A third possibility is 'sodium shift', i.e. a displacement of sodium from the extracellular to the intracellular space with a simultaneous movement of potassium in the opposite direction. The morbidity and mortality associated with HN only arise in cases where the rate of development of HN was 0.5 mmol h-1 or more. Symptoms respond promptly when the HN is quickly corrected with furosemide and 3% sodium chloride.
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PMID:Hyponatraemia in acute brain disease. 132 60

Renal function with respect to water clearance and renal hemodynamics was studied in 15 patients with obstructive jaundice due to cholangiocarcinoma. The results were compared with those of the control normal subjects. There was no change in renal function in the patients with mild to moderate jaundice, with total serum bilirubin from 8.0 to 15.1 mg/dl. Increased urinary sodium excretion and decreased free water and negative water clearances were observed in the patients with severe jaundice with total serum bilirubin from 27.0 to 40.4 mg/dl and normal serum albumin. Renal blood flow was normal, but creatinine clearance was decreased. In severely jaundiced patients with serum bilirubin from 30.5 to 40.1 mg/dl and hypoalbuminemia urinary sodium excretion, free water clearance, negative water clearance, renal blood flow and creatinine clearance were decreased. There was salt and water retention in this group. The findings suggest that in severe jaundice there is inhibition of sodium chloride reabsorption in the thick ascending limb of Henle's loop. ADH and increased hydraulic conductivity of the collecting tubules possibly contribute to decreased free water clearance. In severely jaundiced patients with hypoalbuminemia this salt losing effect is converted to salt retention by increased proximal tubular reabsorption of sodium.
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PMID:Renal function in obstructive jaundice in man: cholangiocarcinoma model. 217 56

Some days after the administration of a third bolus of ABVD (adriamycin, bleomycin, vinblastine, dacarbazine) a patient affected by immunoblastic lymphoma underwent a neurotoxic crisis. The episode lasted 1 week and was followed by a dramatic fall in plasma sodium (104 mEq I-1), associated with a proportionally lesser decrease in plasma chloride and phosphate. Despite the lowest plasma osmolality, detectable levels of circulating ADH were present. After 36 h the hyponatremic episode improved after the infusion of hypertonic sodium chloride. Nevertheless the patient lapsed into a hypotonic coma. The urinary concentrations of the main tubular enzymes (gamma-glutamyltranspeptidase, N-acetyl-glucosaminidase, alpha-glucosidase) proved very high and successively decreased slowly. The most likely cause of such hyponatremic episode is vinblastine. The drug acted through: (a) an already known inappropriate release of ADH, and (b) a hitherto unreported tubular lesion, which impaired the reabsorption of sodium and other coupled solutes.
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PMID:Life-threatening hyponatremia caused by vinblastine. 245 36

A morphometric study was undertaken to quantitate the morphologic changes induced by ADH availability in the rat kidney. Homozygous Brattleboro rats with hereditary diabetes insipidus (DI) (no ADH) were compared to heterozygous Brattleboro control rats (HZ) and to DI rats after 5 to 6 weeks of continuous ADH infusion by implantable Alzet osmotic minipumps (TDI). ADH resulted in a 37% increase in mass of kidney per unit body wt. All kidney zones and all nephron segments were not increased uniformly. The inner stripe was enlarged more than other renal zones. It represented 15.5 +/- 0.7% of the total kidney height along the cortico-papillary axis in DI and 22.2 +/- 1.5% in TDI (P less than 0.025). The volume of the inner stripe in DI and TDI amounted to 10.9 +/- 0.9 and 18.0 +/- 1.0% of the total kidney volume, respectively (P less than 0.001). Selective increases in tubular diameter and cell height, due mostly to an hypertrophy of pre-existing cells, were observed in the earliest part of the thick ascending limbs (TAL) in the inner stripe, resulting in a twofold increase in epithelial volume per unit tubular length (P less than 0.001). Volume density of mitochondria and surface density of basolateral membranes were unchanged but, due to the increase in cell volume and inner stripe thickness, the amount of mitochondria and the surface area of basolateral membrane in the TAL were more than tripled in the inner stripe of treated rats. These changes provide a much greater salt transport capacity in the TAL of treated rats. They probably represent an adaptation of the early TAL to an enhanced sodium chloride transport in response to a direct ADH stimulation and/or to an increased salt delivery to this segment in the concentrating kidney.
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PMID:Selective ADH-induced hypertrophy of the medullary thick ascending limb in Brattleboro rats. 406 80

1. Electrical recordings were made from antidromically identified supraoptic and paraventricular units during intracarotid injections of hypertonic and isotonic sodium chloride solutions in rats.2. The blood concentrations of vasopressin and oxytocin were estimated by bio-assay before and at different intervals after similar injections.3. Although a significant change in the action potential activity of the supraoptic nucleus was associated with hormone release, the results were not entirely consistent with a simple relationship between action potential activity and hormone secretion. Firstly, although some units were excited by the stimulus a substantial number were inhibited. Secondly, the blood concentration of the hormones, particularly ADH, remained elevated for longer than might have been expected if additional hormone had ceased to be secreted as soon as firing rates had returned to control values.4. There were substantial differences between the initial blood concentrations of vasopressin and oxytocin but the firing rates of units in the supraoptic and paraventricular nuclei appeared to be the same.5. Although significantly less paraventricular than supraoptic units were affected by hypertonic injections the blood concentration of oxytocin was increased by a factor of 8 whereas that of vasopressin was increased by a factor of 2.7.
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PMID:Oxytocin and ADH secretion in relation to electrical activity in antidromically identified supraoptic and paraventricular units. 557 37

We have previously suggested that inhibition of renin release by sodium chloride is related to absorptive chloride transport in the loop of Henle. Infusion of sodium chloride fails to inhibit renin release in the adrenalectomized (Adx) rat, and dexamethasone restores renin responsiveness to sodium chloride. The purpose of the present study was to evaluate the relationship between loop function (urinary diluting and concentration capacity) and plasma renin concentration (PRC) in the Adx rat. After hypotonic sodium chloride infusion, free water clearance (CH2O) of Adx rats (0.56 ml/hr/100 g +/- 0.17 SE) was decreased (p less than 0.01) compared to controls (2.86 ml/hr/100 g +/- 0.29 SE); PRC of Adx rats (61.9 units/ml +/- 11.2 SE) was increased (p less than 0.01) above controls (6.0 units/ml +/- 1.7 SE). These differences persisted after administration of d(CH2)5Tyr(Et)VAVP, a potent ADH antagonist. In separate groups of animals, after water deprivation, urine concentration of Adx rat (1,401 mOsm/kg +/- 45 SE) was less (p less than 0.01) than that of controls (2,117 mOsm/kg +/- 169 SE). Dexamethasone normalized both CH2O and urinary concentrating ability and also decreased PRC in Adx rats. Thus, in the glucocorticoid deficient rat, increased renin release is associated with impaired loop function. The loop defect may account for high PRC that is not suppressed by sodium chloride.
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PMID:Mechanism of increased renin release in the adrenalectomized rat. Adrenal insufficiency and renin. 633 60


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