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)

In 3 cases of severe twin transfusion syndrome we demonstrate that the concentration of atrial natriuretic factor (ANF) in the cord blood of recipient twins is significantly elevated compared to that of donor twins. The discrepancy between recipient and donor concentration correlates with the volume of transfusion. The following pathophysiological mechanism for explaining polyhydramnios in recipient twins is proposed: chronic overload in recipient twins causes enhanced release of ANF from the fetal heart. Consequently, increased fetal urine production leads to polyhydramnios, which is additionally enhanced by inhibition of ADH release.
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PMID:Pathophysiology of polyhydramnios in twin transfusion syndrome. 138 87

Pathophysiological mechanisms are reviewed concerning the onset and the perpetuation of the clinical features of congestive heart failure. This syndrome is a severe condition of poor prognosis and bad life quality which in the last decades has reached, in the western industrial countries, the highest levels of general mortality, mainly due to the high prevalence of hypertensive and ischaemic myocardiopathies in the last years. To the clinical features of heart failure mainly contributes a deregulation of the physiological compensatory mechanisms contemporarily and concurrently activated following the primary deficiency of the heart pump function. In physiological conditions, following the myogenic adapting mechanisms reflex mechanisms intervene, activated by intracardiac and aortic and carotid-sinus mechanoreceptors following the variations in intracardiac and intravascular pressure and generally evoking negative feed-back effects. In patients with heart failure arterial high pressure mechanoreceptors respond to the reduction in effective arterial pressure thus provoking a deactivation of the tonic inhibition on the sympathetic cardiovascular drive. This leads to an activation of peripheral and renal vasoconstrictor tone, to a raised medullary catecholamine incretion, to heart rate and inotropism stimulation, and to an increase in pituitary gland ADH production as well as to an activation of renin-angiotensin-aldosterone system (RAAS). Analogous vasoconstrictive, and sodium and water retentive effects can be elicited by endothelin produced by endothelial cells and found in high plasma levels in CHF. These excitatory effects, leading to a rise in systemic vascular resistance and to hydro-electrolytic retention with volume expansion, are not efficiently counteracted by the opposite effects triggered by cardiopulmonary vagally mediated mechanoreceptors activated by the raised cardiac filling pressure and leading to sympathetic nervous inhibition, peripheral and renal vasodilation, ADH and RAAS inhibition. Analogous effects should be provoked by the raised production, due to enhanced heart wall distension, of atrial natriuretic factor leading to vasodilation, natriuresis and diuresis. Reduced sensitivity of cardiopulmonary baroreceptors and lowered production of ANF due to structural cardiac changes could represent, according to most opinions, the main factors responsible for the prevailing sympathetic activation and hydro-saline retention in CHF. The activation of cardiopulmonary sympathetic positive-feed back afferents, could be also involved in the characteristic alteration of the vago-sympathetic balance in heart failure. The persistent reduction in heart pump function could lead to the instauration of vicious circles among the various regulatory systems and create an overcompensation condition.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[The physiopathological aspects and new therapeutic approaches in cardiac-circulatory failure]. 149 59

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

There appears to be two distinct natriuretic factors. One group, suspected since 1951 in overloaded dogs, had a low molecular weight: it belongs great affinity for ouabain, binds to digoxin antibodies and inhibits NA-K ATPase; this group seems heterogeneous in spite of the extraction of an amino glucosteroid-like substance from human urines. These factors are vasoconstrictor; the source is not still well known (hypothalamus ?). The atrial natriuretic factor (ANF) is a peptide about 20 to 25 amino acids and comes from a precursor of 152 amino acids, its synthesis was successful; secreted in the plasma from endocrine atrial granules, it causes striking natriuresis and diuresis and relaxes vascular and intestinal smooth muscle; it acts on guanylate cyclase but its renal mechanism of action is not well known; it constitutes an antagonist axe to ADH and RAA system. The relations between the two groups of natriuretic factors do not seem still very clear.
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PMID:[Natriuretic factors]. 295 21

The effects of intracerebroventricular (ICV) infusion of atrial natriuretic factor (ANF; atriopeptin III) on renal function, plasma concentrations of antidiurectic hormone, aldosterone, and plasma renin activity (PRA) were examined in anesthetized rats and sodium-depleted conscious sheep. The results were compared with those obtained by intravenous infusion of the same dose of ANF. In both rats and sheep, urine volume was increased four- to sixfold over basal values by ICV infusion of ANF. The response was not associated with increased excretion of sodium or potassium. However, urine osmolality was decreased, and free water clearance increased. Intravenous infusion of the same dose of ANF was without effect. Neither mean arterial blood pressure nor heart rate was changed by the ICV infusion of ANF. In the sheep, renal plasma flow showed no significant changes and glomerular filtration rate was unaltered with the exception of a single experimental period out of four periods of ICV ANF infusion. Plasma concentration of ADH was decreased and PRA increased, whereas aldosterone levels remained unchanged as a function of ICV ANF. In the rat, the diuretic response to ANF was prevented by continuous intravenous infusion of a subpressor dose of ADH. These results suggest that ANF within the central nervous system inhibits secretion of ADH.
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PMID:Centrally administered atrial natriuretic factor increases renal water excretion. 295 69

After overnight food and fluid restriction, seven healthy old (62-74 yr) and eight young (21-28 yr) men were examined before, during, and after 3-h head-out immersion (HOI) in thermoneutral water (34.5 +/- 0.5 degrees C). On separate days, all subjects remained seated in air for 5 h to obtain the time control data. Although HOI induced a reversible increase in urine flow in all subjects, the response was faster and greater in magnitude in the elderly than in the young. Na excretion and osmolal clearance also followed a response pattern identical to that of urine flow; thus the HOI-induced diuresis was entirely osmotic. Endogenous creatinine clearance increased in the elderly at 2 h of HOI, suggesting an age-related modification in kidney hemodynamics. Although there was virtually the same cephalad blood shift (measured by impedance cardiography), mean arterial pressure significantly increased (P less than 0.05) during HOI in the elderly, which also indicated a different response of peripheral circulation to HOI in the elderly. Control level of plasma atrial natriuretic factor (ANF) was nearly twofold greater in the elderly compared with the young. The HOI induced a nearly fourfold increase in ANF in the elderly, whereas that for the young was threefold. Both plasma aldosterone and ADH responses to HOI were attenuated in the elderly compared with the young, which had no correlation with urine flow or Na excretion. It is concluded that the elderly release more ANF at a given cephalad volume expansion compared with the young, but the vasodilative reaction to ANF was attenuated in the elderly.
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PMID:Renal and endocrine responses in the elderly during head-out water immersion. 296 55

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

A 64-year-old Japanese male was admitted to Kotoh General Hospital because of fever and cough on July, 14, 1997. Laboratory data showed hypereosinophilia (11,500/microliter) and high titer of anti-myeloperoxidase antineutrophil cytoplasmic antibody (319 EU). A physical examination revealed progressive peripheral neuropathy. He had been diagnosed as having bronchial asthma since November, 1996. Therefore, he was diagnosed as having Churg-Strauss syndrome (CSS). He was treated with methylprednisolone pulse therapy (500 mg/day for 3 days) and oral prednisolone (PSL, 60 mg/day). However, peripheral neuropathy was rapidly progressive, and echocardiogram revealed cardiac hypofunction (ejection fraction (EF); 39%). He was refereed to Akita University Hospital for further examination. On admission, laboratory data showed hyponatremia (125 mEq/l) with inappropriate secretion of antidiuretic hormone (ADH, 13.0 pg/ml). Atrial natriuretic peptide was normal (26 pg/ml). Urinary osmorality was 488 mOsm/l, and urinary sodium excretion was 86 mEq/l. Renal, adrenal, and thyroid functions were normal. From these data, his hyponatremia was caused by syndrome of inappropriate secretion of ADH (SIADH). After cyclophosphamide-pulse therapy (500 mg) and oral administration of cyclophosphamide (50 mg/day) and PSL (50 mg/day), peripheral neuropathy improved gradually, and his serum sodium returned to normal, but cardiac hypofunction continued. A possible relationship between SIADH and CSS is discussed.
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PMID:[Severe peripheral neuropathy, cardiac hypofunction, and syndrome of inappropriate secretion of antidiuretic hormone (SIADH) in a patient with Churg-Strauss syndrome]. 1061 73

VPA-985 is an orally active, competitive vasopressin V(2) receptor antagonist that in normal human beings increases water excretion without affecting solute excretion. Whether solute excretion is affected in patients with hyponatremia resulting from inappropriate secretion of antidiuretic hormone (SIADH) or from cirrhosis treated with VPA-985 is unknown. Six hyponatremic patients with SIADH and 5 hyponatremic patients with cirrhosis with ascitis (CWAs) were treated with 50 or 100 mg VPA-985 twice daily. Evolution of creatinine, urea, uric acid, sodium, potassium, and osmotic clearance were determined. Volume hormones (plasma renin [PR], aldosterone, antidiuretic hormone [ADH], atrial natriuretic factor [ANF]) were also determined before and after treatment. In patients with SIADH, serum sodium concentration (SNa) was generally corrected in 1 day (SNa: 126 +/- 4.5 mmol/L at t = 0 hours and 133 +/- 5.6 mmol/L at t = 24 hours) and associated with a decrease in sodium excretion (from 82 +/- 22 mmol/24 hours to 45 +/- 21 mmol/24 hours; P < 0.05) without modification in potassium excretion. Despite an increase in diuresis (from 0.84 +/- 0.2 ml/min to 1.46 +/- 0.4 ml/min) urea and uric acid clearances decreased. Urine osmolality decreased from 414 +/- 148 mOsm/kg H(2)O to 209 +/- 55 mOsm/kg H(2)O. Volume hormones did not change. In the CWAs the rise of SNa was more progressive (SNa: 126 +/- 2.8 mmol/L at t = H0 to 133 +/- 4.9 mmol/L at t = 48 hours) and parallel to an augmentation in sodium excretion (from 23 +/- 18 mmol/24 hours to 65 6 60 mmol/24 hours the second day of VPA administration). The higher sodium excretion was also connected with a progression in potassium excretion (from 22 6 7 mmol/24 hours to 36 +/- 18 mmol/24 hours). The increase in diuresis under VPA from 0.42 +/- 0.2 mL/min to 1.7 +/- 0.9 mL/min resulted in a higher urea clearance. Urine osmolality decreased from 509 +/- 142 mOsm/kg H(2)O before VPA to 194 +/- 106 mOsm/kg H(2)O after VPA. ADH increased in CWAs treated with VPA, from 1.9 +/- 1.2 pg/mL to 5.3 +/- 2.8 pg/mL (P <.05) while other volume hormones did not change. VPA-985 is a highly effective drug in the short-term management of hyponatremic patients with SIADH or CWAs. SNa correction is associated with urinary sodium retention in SIADH, whereas in CWAs a mild increase in sodium excretion is observed.
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PMID:Difference in solute excretion during correction of hyponatremic patients with cirrhosis or syndrome of inappropriate secretion of antidiuretic hormone by oral vasopressin V2 receptor antagonist VPA-985. 1175 87