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Query: UMLS:C1332347 (ADH)
 2,230 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Because of the inaccessibility of the thick ascending limb (TAL) to micropuncture, it has been difficult to evaluate the effects of ADH and atrial natriuretic factor (ANF) on TAL salt transport in vivo. The purpose of the present study is to assess the effects of these hormones on TAL NaCl reabsorption in vivo. Although passive NaCl permeability and unidirectional Na fluxes were not measured, the microstop-flow conductivity technique that was used in these studies controls solute delivery, permits the measurement of the rate of net NaCl reabsorption, and tests the capacity of the TAL to establish a limiting gradient. Despite the presence of a dramatic natriuretic response, a natural extract of ANF did not significantly increase the minimum NaCl concentration reached by the TAL after 60 s of stop-flow. However, 1-[desamino]-8-D-arginine vasopressin (dDAVP) increased by 23%, the rate at which luminal Na concentration declined, and reduced by 28% the minimum NaCl concentration achieved by the TAL. Therefore, these results do not demonstrate a significant direct peritubular effect of ANF on TAL NaCl permeability in outer cortical nephrons, but support a role for antidiuretic hormone in enhancing TAL NaCl reabsorption in vivo.
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PMID:Thick ascending limb response to dDAVP and atrial natriuretic factor in vivo. 295 Jul 72

Competitive antagonists of the antidiuretic (ADH) activity of vasopressin were first described some six years ago. When studied in vitro, ADH antagonists displace vasopressin from specific renal binding sites and antagonize, in a competitive fashion, vasopressin stimulation of adenylate cyclase and transepithelial water, salt, and urea fluxes. When studied in vivo, the ADH antagonists increase renal water excretion and antagonize, in a competitive fashion, the ADH activity of vasopressin. Marked species heterogeneity is apparent with ADH antagonists in vivo, and inconsistencies between in vitro and in vivo findings within the same species are reported. Other renal responses associated with administration of ADH antagonists include changes in renal hemodynamics and renal salt and urea excretion. The effects on salt excretion appear to be limited to those species in which vasopressin stimulation of epithelial salt reabsorption has been demonstrated. In summary, the role of vasopressin as the principal factor regulating renal water handling is supported by experience with ADH receptor antagonists. However, that experience also indicates the emerging significance of autocoids, and other synergistic factors, to affect ADH receptor/effector mechanisms and to modulate renal ADH responses.
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PMID:Antagonists of the antidiuretic activity of vasopressin. 296 1

CHF may activate the RAS by various mechanisms. Acute CHF is associated with high PRA, whereas chronic, stable disease is combined with normal values. The response to ACEI is affected by blood pressure, degree of activation of the RAS, salt balance and degree of possible renal failure. It may also be affected by concomitant diuretic or, e.g., digoxin therapy. ACEI improves RPF, GFR may remain normal or may increase, if it was previously impaired due to reduced RPF. Severe hypotension in combination with decreased autoregulatory capacity may decrease GFR. Generally, renal excretion of sodium and water increase. These changes in renal handling of salt and water are primarily caused by decreased AII. They are also augmented by inhibited sympathetic tone and thirst and decreased release of ADH and aldosterone. Increased synthesis of vasodilating and natriuretic PGs is probably also of some importance. Dilutional hyponatremia may be corrected by combined ACE inhibitor and furosemide treatment. Water and sodium excretion increase and sodium is redistributed from the intracellular space. Low serum sodium values increase and azotemia may be corrected, if ACE inhibitor doses are carefully titrated to avoid severe hypotension. These effects are ascribed mainly to a decrease of AII, thirst and ADH release. The effect of furosemide is improved since increased amounts of salt are delivered to the loop of Henle and access of furosemide to its site of action is facilitated by increased RPF. ACEI does not cause any obvious negative effects on renal handling of salt and water.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of ACE inhibition on renal regulation of salt and water. 301 59

Previous experiments in Brattleboro rats with hereditary diabetes insipidus revealed that absence of ADH led to several alterations in kidney anatomy, which could be reversed by chronic ADH treatment. Present experiments were undertaken to determine if similar alterations were observable in normal Wistar rats when endogenous ADH level was varied by manipulating water intake or when exogenous ADH was infused. Water intake was increased by giving food with a high water content ad libitum and offering 5% glucose solution to drink (HWI rats), or decreased by reducing water intake to 1/3 of spontaneous intake (RWI rats). An additional group received chronic ADH infusion with Alzet osmotic minipumps (ADH rats). Results were compared to those obtained in control rats (CON) drinking ad libitum. RWI, CON, and ADH rats ate dry pellets ad libitum. After 6 weeks on these regimens kidneys were perfusion fixed and serial sections were cut for morphometric measurements by light microscopy. Results in the four groups showed that kidney weight relative to body weight was influenced by the operation of urinary concentrating mechanism, with HWI less than CON less than RWI less than ADH. The increase in kidney weight in rats with high urine concentration was not homogeneously distributed throughout the different kidney zones and the different nephron segments. The inner stripe of the outer medulla (IS) increased more in relative height and volume than other kidney zones and, within this zone, the volume of epithelium of thick ascending limb of Henle's loops (TAL) increased more than expected from the whole kidney weight increase. In outer stripe of outer medulla (OS) and in cortex (C), TAL hypertrophy was equal to or lower than expected from whole kidney weight increase. Collecting duct epithelium in C, OS, and IS increased in proportion to whole kidney weight. The MTAL hypertrophy in IS was due to an increase in size of preexisting cells, except in the ADH group where an increase in cell number was also observed. Internephron heterogeneity with regard to glomerular size was greater in RWI and ADH than in CON and HWI rats. The marked hypertrophy of the deep TAL in the IS of rats in which urine concentration was stimulated could be related to an increase in salt transport in this nephron segment, triggered both by a direct stimulation by ADH, and by an increased salt recycling. The elongation of the inner stripe provides a greater length for the operation of the countercurrent multiplier system responsible for building up of the osmotic pressure gradient in the medulla.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Adaptation of the rat kidney to altered water intake and urine concentration. 317 86

This prospective study is based on 256 patients with severe brain injury. Six patients (2.3%) developed the clinical picture of inappropriate secretion of antidiuretic hormone (SIADH): 3 in the first 3 days following the injury, 3 after more than a week. Their ADH plasmatic level were measured by radio-immunoassay. In the former, many factors, largely iatrogenic, can explain the increased secretion of ADH we found and which is then definitely "appropriate". It should be prevented by fluid restriction. In the latter, we found adequately low ADH levels, when the hypo-osmolarity is taken into account. Here, the aetiology seems to be a renal salt loss, eventually in relation to a natriuric factor (e.g. atrial natriuretic factor), justifying the term: "Cerebral salt wasting syndrome". With the resistance to fluid restriction, the treatment still remains a problem.
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PMID:Hyponatremia hypo-osmolarity in neurosurgical patients. "Appropriate secretion of ADH" and "cerebral salt wasting syndrome". 339 48

Tubuloglomerular feedback is an intrarenal control mechanism designed to regulate the amount of salt entering the distal nephron. Its regulatory efficiency depends upon the magnitude of the vascular response to changes in the luminal signal (the feedback relationship) and on the adjustments in proximal absorption, which determine the macula densa signal (the feedforward relationship). Studies of the feedback relationship have established that the vascular response is related to macula densa solute concentration in a sigmoidal fashion, with the normal operating point located somewhere in the steep portion of the curve. Thus, tubuloglomerular feedback tonically suppresses glomerular filtration rate, an effect that may be even more pronounced in juxtamedullary nephrons. An alteration in the feedforward function and thus in the macula densa signal is likely to participate in the vascular resistance changes initiated by changes in arterial pressure, elevated protein intake, or ADH administration. Our understanding of the intra- and intercellular mechanisms underlying information transfer across the JGA is currently incomplete, but there is some information about the biochemical characteristics of the cellular components. The enzymatic and surface properties establish the distinct nature of the macula densa cells and indicate a distinct function.
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PMID:The tubuloglomerular feedback mechanism: functional and biochemical aspects. 355 1

The biochemical features of severe hyponatraemia due to thiazide administration in 7 non-oedematous patients were compared with those in hyponatraemia due to frusemide. Hypouricaemia has been shown to occur in hyponatraemia due to the syndrome of inappropriate antidiuretic hormone activity and this was measured along with fractional uric acid clearances in all the patients. Five of the patients had been on thiazides (or hydrochlorothiazide with amiloride) for only a few days to a few weeks. Fractional uric acid clearance was elevated and serum uric acid levels were low in five of them and returned to the normal range on restoration of serum sodium to normal. By contrast, the patients on frusemide did not show any abnormality in fractional uric acid clearance at any stage. These results are consistent with excess ADH activity as having caused hyponatraemia induced by thiazides in 5 of the 7 cases, whereas frusemide caused a sodium depletion syndrome. Treatment in the former cases is by water restriction, and in frusemide-induced salt depletion by saline supplementation.
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PMID:Significance of the measurement of uric acid fractional clearance in diuretic induced hyponatraemia. 377 74

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. Previous work has demonstrated that the cat heart secretes a substance which resembles the 18-monoacetate of D-aldosterone (18 MA) in chromatographic properties and biological actions. This substance (HS) releases ADH from the neurohypophysis and, in higher concentration, causes renal retention of salt and water. HS is extracted from blood, separated chromatographically and assayed in terms of equivalent 18 MA activity either by inhibition of water diuresis in rats or by reduction of the excretion of Na by the isolated kidney. Positive correlation has been demonstrated between heart rate and HS secretion.2. Heart-lung preparations from cats have been used to disclose additional factors controlling the rate of secretion of HS from heart muscle.3. Positive inotropic effects produced by administration of digoxin or adrenaline or by increase in peripheral resistance are associated with increases in the secretion of HS.4. Negative inotropic effects produced by high concentrations of procaine hydrochloride or by increase in venous return without change in external work are associated with decrease in HS secretion.
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PMID:Factors controlling the secretion of a substance biologically resembling the 18-monoacetate of D-aldosterone by heart muscle. 549 21

The effect of i.v. Pitressin (ADH) in a dose of 1 U/hr on permeability characteristics and on absorptive capacity of the normal human small intestine was investigated. The method of continuous intestinal perfusion was employed with polyethylene glycol 4000 as a nonabsorbable marker. Unidirectional flux rates of Na and H(2)O were calculated from the disappearance of (22)Na and of (3)HOH from isotonic saline solution within the intestinal lumen. Each study consisted of two successive perfusion periods: one while the subject was hydrated, the other during ADH infusion or while the subject was dehydrated. Water and sodium absorption from isotonic NaCl occurred in the hydrated state and was abolished by ADH as well as by dehydration in the jejunum. In some instances, net gain of water and sodium in the lumen occurred. In the ileum, ADH and dehydration caused a decrease in water and sodium absorption rate. By contrast, unidirectional flux into the intestinal lumen of water and sodium, as well as dextrose and D-xylose diffusion, remained unchanged by ADH. During perfusions with hypertonic urea solutions the rates of sodium and water entry into the intestine were greatly increased during i.v. ADH infusion, whereas urea loss from the study segment remained constant. ADH in the dosage used did not affect human intestinal motility. The results suggest that circulating ADH in physiologic concentrations affects the small intestine in one of two ways: increased secretion of water and salt into the lumen or direct interference with the active sodium transport mechanism.
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PMID:Effect of antidiuretic hormone on human small intestinal water and solute transport. 564 53


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