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 anesthetized dogs, perfusion of the cerebral ventricles with indomethacin (IM), an inhibitor of prostaglandin biosynthesis, at rates of 1.9 or 7.6 microgram/min was without effect on the plasma ADH concentration. Ventriculo-cisternal perfusion with angiotensin II (AII; 19 ng/min) resulted in a 3-fold increase in the plasma ADH concentration within 45 min. When AII and IM were perfused together, the plasma ADH concentration increased only 2-fold, a response which was significantly lower than that obtained with AII alone. Thus, the ability of central AII to stimulate ADH release may depend, at least in part, upon the local release of prostaglandins.
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PMID:Effect of ventriculo-cisternal perfusion with angiotensin II and indomethacin on the plasma vasopressin concentration. 65 25

1. Tonicity dominates the release of ADH with similar sensitivities (0.2-1 pg/ml per mOsm/kg) for both birds and mammals. 2. There is an inverse relationship between the volume of the extracellular fluid compartments and the plasma level of ADH. 3. Angiotensin II formation is governed by volume factors. 4. In birds the factors reducing the delivery of Na+ to the nephron distal tubules stimulate ANGII formation. 5. Mammals have a high vascular constrictor sensitivity to ADH and ANGII; there is little or no vascular sensitivity to these in birds. 6. In birds and mammals the subfornical organ and other circumventricular organs have receptors that specifically bind ANGII. 7. Dog and duck CSF levels of ADH and AII indicate their function as specific mediators of intrinsic neuronal systems controlling salt and fluid balance.
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PMID:Central and systemic antidiuretic hormone and angiotensin II in salt and fluid balance of birds as compared to mammals. 290 89

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

Drinking in response to peripheral osmotic stimuli has been shown to be initiated via an osmoreceptor mechanism. Andersson and his colleagues, from work in the goat, have challenged this hypothesis. They have found that the CSF concentration of Na is the most important factor and that an increase causes thirst, ADH release, and a decrease in Na sodium appetite. We have investigated this subject using pigeons since they have large cerebroventricular spaces and are very rapid drinkers. Pigeons were found to respond normally to peripheral osmotic stimuli but only hypertonic NaCl centrally. Central infusions of water inhibited drinking in response to simultaneous i.v. infusions of 0.5 M NaCl or 1.0 M sucrose. The inhibition occurred only during the infusion and drinking recovered rapidly to normal shortly afterwards. Hypertonic sucrose (0.9 M) centrally inhibited drinking to the same peripheral stimuli whereas 0.3 M sucrose centrally blocked drinking only during i.v. infusion of 0.5 M NaCl but not i.v. 1.0 M sucrose. Drinking recovered rapidly after the infusion. Hypertonic NaCl centrally potentiated drinking to peripheral osmotic stimuli. Urine and electrolyte excretion was increased after hypertonic sucrose infused simultaneously i.c.v. and i.v. compared with other solutions infused i.c.v. and hypertonic sucrose i.v. Drinking induced by AII centrally was additive with hypertonic NaCl centrally. AII infused centrally in water halved the drinking response. AII infused peripherally was not affected by central decreases in Na but additive with increases. Thus there appears to be a central receptor mechanism for Na but it seems to act as a "permissive gate", rather than a potentiator, regulating drinking in response to peripheral or central osmotic stimuli or AII.
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PMID:A central Na+ receptor and its influence on osmotic and angiotensin II induced drinking in the pigeon Columbia livia. 644 27