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

The temperature of the anterior and middle hypothalamus of conscious Pekin ducks was altered with chronically implanted thermodes. Both urine formation and salt secretion by the supraorbital glands were influenced by hypothalamic cooling. When osmotic diuresis was induced by continuous intravenous infusion of 1.2 ml . min-1 of 293 mosm . kg-1 mannitol in H2O solution, hypothalamic cooling increased urine flow rate at reduced urine osmolality and unchanged osmolal excretion rate. The degree of this cold induced diuresis increased with cooling intensity. Additional ADH administration by continuous infusion at a supramaximal dose abolished the diuretic effect of hypothalamic cooling. When water diuresis was induced by intragastric continuous infusion of 1.2 ml . min-1 of distilled water, hypothalamic cooling enhanced the diuresis, but hypothalamic warming had equivocal effects. The diuretic effects of hypothalamic cooling suggest an inhibition of endogeneous ADH release by lowering hypothalamic temperature. When the salt glands of salt adapted ducks were stimulated by continuous intravenous infusion of 0.2 ml . min-1 of 800 mosm . kg-1 NaCl in H2O solution, hypothalamic cooling reduced the salt gland secretion rate to an extent depending on cooling intensity. It is concluded that the activities of those integrative and/or efferent hypothalamic neurons, which mediate the hormonal control of renal water absorption and the nervous control of salt secretion by the supraorbital gland, depend on their own temperature.
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PMID:Hypothalamic temperature and osmoregulation in the Pekin duck. 57 Oct 87

Post-traumatic diabetes insipidus was observed in 14 among 702 patients with severe trauma. The cause of the abnormal vasopressin secretion may be cerebral oedema, cerebral contusion near the hypothalamus, pull on the hypophyseal stalk by displacement or gross destruction of the brainstem. The hormonal hypofunction disappears once the cerebral damage has regressed. Treatment consists of exact balancing of water and electrolyte loss, using salt-free solutions. Drug treatment with vasopressin and with ADH-secretion stimulators has given unsatisfactory results, but should be used. Seven of the 14 patients died of their injuries. The symptoms of the diabetes insipidus syndrome regressed in the survivors.
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PMID:[Post-traumatic diabetes insipidus syndrome (author's transl)]. 62 50

1. In acute experiments, high levels of endogenous prostaglandins, provoked by operative stress, could obscure or alter the actions of infused prostaglandins on the kidney. For this reason we decided to compare the effects of infusing prostaglandin E(1) into the renal artery of the dog before and after the administration of phenylbutazone, a prostaglandin synthetase inhibitor.2. Infusion of prostaglandin E(1) into the left renal artery of the pre-phenylbutazone treated dog undergoing a mannitol diuresis increased renal plasma flow, glomerular filtration rate and the excretion of salt and water. The findings are in general agreement with those reported by others.3. Following phenylbutazone administration the vascular and saluretic actions of prostaglandin E(1) were unchanged but a reduced diuretic effect was observed. The response to a low dose of prostaglandin E(1) (0.05 mug/min) was reduced from 1.46 +/- 0.15 to 0.96 +/- 0.16 ml./min (P < 0.001) and the response to a high dose (0.5 mug/min) from 1.82 +/- 0.19 to 0.99 +/- 0.31 ml./min (P < 0.002).4. A significantly less dilute urine was excreted during prostaglandin infusion in the dog after phenylbutazone treatment than before. The reduction in the diuretic response was of the same order as the decrease in the free water clearance response, while the increase in osmolar clearance was unchanged.5. In water-loaded dogs treated with phenylbutazone, infusion of prostaglandin E(1) into the left renal artery had a biphasic effect on urine output from the left kidney. An initial diuretic response to a low dose of prostaglandin E(1) disappeared with the infusion of higher doses, and antidiuresis developed in the immediate post-infusion period.6. As prostaglandin was infused into the left kidney progressive antidiuresis was seen in the non-infused right kidney.7. It is concluded that endogenous prostaglandins do not obscure or alter the vascular and saluretic actions of intrarenal prostaglandin E(1). The findings question the proposed link between the vascular and saluretic actions of this compound.8. It is suggested that the reduced diuretic effect of prostaglandin E(1) in series no. 1, and the antidiuresis in the water-loaded dogs, are caused by the release of endogenous ADH. It is further suggested that phenylbutazone unmasks this release by removing the endogenous prostaglandins. If these deductions are correct, the findings support the anti-ADH role assigned to endogenous prostaglandins by Anderson, Berl, McDonald & Schrier (1975).
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PMID:A bilateral antidiuresis to renal artery infusion of prostaglandin E1 in dogs treated with phenylbutazone. 70 55

The water metabolism was studied in homo- and heterozygous Brattleboro rats suffering from hereditary hypothalamic diabetes insipidus. In homozygous Brattleboro rats the spontaneous water intake and urinary output and the diuretic reactions signficantly increased after water and salt loading. No antidiuretic activity was found in the urine, posterior pituitary or hypothalamus of these animals, and this state was not affected by hyperosmosis. For the heterozygous rats the spontaneous water intake and urinary output and the diuretic reaction exceed the respective control values, the posterior pituitary, the hypothalamus and the urine are of reduced antidiuretic activity and this activity is less mobilizable by hyperosmosis. It is concluded that the ADH-reserve deficiency is total in the homozygous Brattleboro rats, and partial in the heterozygotes. As a result of hyperosmosis, the vasopressin release is of a reduced extent, yet detectable in the heterozygotes.
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PMID:The ADH-reserve capacity in Brattleboro rats. 74 41

The literature on hydronatriuresis control processes operating at the level of individual renal functional units and of the organ as a whole is analysed. 1) Elementary sodium salt and water tubular transport mechanisms. In converting the filtrate into urine, the kidney expends metabolic energy: this is used in the (active) transport of sodium salts; (passive) transport of water takes place along the osmotic gradients created by salt transfer. The proximal tubules reabsorb the sodium bic-rbonate actively. The reabsorption of the osmitic equivalent of water has the effect of concentrating NaCl in the tubular fluid. An important role in the reabsorption of NaCl is played by passive diffusion from the lumen to the interstitial fluid; the remainder is transferred actively, perhaps by an electrically neutral pump. With respect to the other nephronic segments, the proximal tubule has a relatively high passive permeability to water and salts: active transport here must not surmount high friction resistances nor take place against important concentration gradients. The low permeability of the distal nephron, on the other hand, increases the energy cost of salt transport; for the same reason, important electrochemical gradients are created and the composition of tubular fluid is drastically altered. 2) Elementary mechanisms of tubular potassium transport. Potassium is reabsorbed actively along the whole nephron by a luminal pump. The proximal tubules and Henle loops promote practically complete absorption of filtrated potassium. The distal tubules and collectors have the two-fold capacity of secreting and reabsorbing cation: the quantity of potassium excreted with the urine depends on the degree of excess of the secretion process. At distal tubular level, potassium secretion is a passive phenomenon dependent on the favourable transluminal gradient of the cation's electrochemical potential. 3) Renal function and volume homoeostasis of extracellular fluid. The organism's sodium content is largely controlled by renal excretion of sodium; homoeostasis of the sodium mass guarantees volume homoeostasis of the extracellular fluid through thirst and osmotic secretion of ADH. Extracellular fluid volume errors are picked up by the organism to the extent to which they translate themselves into pressure variations in the low pressure vascular system or into variations in haematic constituent concentration within the vascular sector, produced with velocities independent, at least in the short term, of the volume of extracellular fluid. In control of natriuria are the glomerular filtrate, intrarenal distribution of blood flow and tubular reabsorption of sodium; in its turn, the latter is subject to nervous and hormonal influences and influences from the physical environment surrounding the nephrons...
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PMID:[Renal water-electrolyte excretion and its control mechanisms. Current status of knowledge]. 99 12

This is a case report involving a 9 year old girl with a teratoma that infaced mainly the bilateral hypothalamus. The girl was observed for 14 months after partial surgical removal. During that time she showed aphagia, adipsia, hypopituitarism, and visual and psychiatric disturbances. Severe hypernatremia also was present, even though large amounts of 5% glucose solution without salt were given I.V. Food and water were given by nasal gastric gavage and later gavage via gastric fistula, but the hypernatremia remained unchanged. When pitressin or spironolacton (anti-aldosterone) were administered, remarkable effect on the hypernatremia couldn't be found. Upon autopsy it was discovered that the bilateral hypothalamus, left subthalamus and ventral part of the thalamus were invaded by teratoma. Comparing many similar clinical reports and manifestations of hypothalamic lesions in experimental animals, it is reasonable to assume that the mechanisms of hypernatremia were caused by the disturbances of ADH secretion, thirst centre and osmoreceptor in the hypothalamus.
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PMID:[Neurogenic hypernatremia caused by a teratoma on the supraoptic region (author's transl)]. 123 50

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

To elucidate the contribution of various hormones and neuromodulators in the central nervous control of body fluid homeostasis, the saltwater-acclimated Pekin duck represents an ideal model due to the cytoarchitecture of its hypothalamus, and the marked systemic and hypothalamic sensitivity of its osmoregulatory system. Employing animal physiology, electrophysiology, histochemistry and receptor binding techniques, the role of angiotensin II (A II) and norepinephrine (NE) as both circulating hormones and neurotransmitters in central osmoregulation through interaction with neuronal targets inside and outside the blood-brain barrier (BBB) could be investigated. Application of both agents into the systemic circulation or into the cerebrospinal fluid of conscious animals, and the monitoring of hypothalamo-neurohypophyseal antidiuretic hormone ADH (= AVT) release, cardiovascular parameters such as mean arterial pressure (MAP) and avian salt gland function allowed to discriminate between actions of A II and NE at sites within or outside the BBB. Of the latter, the median eminence (ME), the subfornical organ (SFO) or the organum vasculosum laminae terminalis (OVLT) are of prime importance. Receptor autoradiography using radioiodinated ligands specific for A II, alpha 1-, alpha 2- and beta-receptors including the pharmacological characterization of these binding sites permit to establish a molecular correlate of the modulatory actions of both A II and NE.
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PMID:Functional hypothalamic angiotensin II and catecholamine receptor systems inside and outside the blood-brain barrier. 141 Apr 29

A study was performed on hydroelectrolytic changes in neurosurgical patients operated for clipping anterior communicating artery aneurysm. The patients were observed during a seven day period in ICU, between the preoperative day and the sixth post-operative day. No statistically significant changes were observed, except for hyponatriemia on the day of surgery. The etiology of this phenomenon is not clear: it could be a change of ADH or "cerebral salt wasting syndrome". A wider number of patients and repeated haematological tests are necessary.
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PMID:[Metabolic and water-electrolyte changes as postoperative complications in aneurysms of the anterior communicating artery]. 162 Apr 65

All hyponatremic states have in common elevation of vasopressin. Without this the loss of salt would be followed by appropriate diuresis and normonatremia. If hyponatremia is triggered by a volume change as in heart failure or portal cirrhosis not only is ADH released but the mechanisms that control salt retention create an essentially sodium free urine, always less than 20 mEq/L. If the initial event is inappropriate ADH secretion whether it be cerebral disease, neoplasm, a pulmonary lesion or a growing list of drugs; there is no related signal for salt retention and urine sodium and tonicity are high, the latter usually higher than that of plasma. If salt loss is due to intrinsic renal disease, diuretics, osmotic or otherwise, or adrenal failure urinary sodium is variable depending upon the magnitude of the response to volume of salt retaining factors. Because hyponatremia is often present with major illness and because more than one factor may be involved in its genesis, the establishment of its origin and appropriate treatment remain a diagnostic and therapeutic challenge.
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PMID:Hyponatremia: manifestations and treatment. 162 51


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