Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.1.1.1 (alcohol dehydrogenase)
 9,284 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Experiments were performed on 54 chronically water diuretic Munich-Wistar rats to investigate the effects of various antidiuretic peptides on the determinants of glomerular ultrafiltration. Transition from water diuresis to antidiuresis, induced either by intravenous infusion of 1) exogenous peptides (Pitressin, synthetic arginine vasopressin, or synthetic [1-deamino,4-valine]-8-D-arginine vasopressin) or 2) dibutyryl cyclic AMP, or by stimulation of endogenous ADH release by acute, mild arterial hemorrhage, was associated with near-constant or decreased values for single nephron (SN) and total kidney GFR. Nevertheless, the glomerular transcapillary hydraulic pressure difference (deltaP) uniformly increased with antidiuresis, due to consistent reductions in Bowman's space hydraulic pressure rather than to increases in glomerular capillary hydraulic pressure, the former a consequence of the fall in urine flow rate. In all antidiuretic states, the rats were uniformly observed to be at filtration pressure disequilibrium, permitting calculation of unique values of the glomerular ultrafiltration coefficient (Kf). These values of Kf in antidiuresis were invariably lower than the values obtained during water diuresis. Whether these effects of ADH and DBcAMP on deltaP and Kf represent physiological influences in the control of GFR remains uncertain; their offsetting effects in the present studies usually failed to alter GFR appreciably.
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PMID:Evidence for glomerular actions of ADH and dibutyryl cyclic AMP in the rat. 19 8

The effects of in vivo physiologic doses of vasopressin and 1-deamino-8-D-arginine vasopressin (DDAVP) on the cyclic AMP content of plasma, urine, and renal papillary tissue were determined in the ADH-deficient Brattleboro rat. During clearance studies, plasma cyclic AMP concentrations and both total and nephrogenous urinary cyclic AMP excretion in vasopressin- and DDAVP-treated rats were similar to the values in time-matched controls. In contrast, in situ renal papillary cyclic AMP content was higher (P less than 0.001) in both vasopressin- (35.7 +/- 3.6 pmol/mg protein) and DDAVP- (29.7 +/- 2.2 pmol/mg protein) treated rats compared to controls (15.1 +/- 1.3 pmol/mg protein). Endogenous stimulation of vasopressin by dehydration in normal rats increased both papillary cyclic AMP content (27.1 +/- 2.7 pmol/mg protein) and urine osmolality, whereas no change in papillary cyclic AMP was observed following dehydration in Brattleboro rats (13.6 +/- 0.8 pmol/mg protein) despite an increase in urine osmolality. The results demonstrate that changes in cyclic AMP following in vivo vasopressin are best demonstrated by measurement of in situ cyclic AMP content of the renal papilla, whereas total urinary cyclic AMP and nephrogenous cyclic AMP are not useful indices of tubular sensitivity to this hormone.
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PMID:Dissociation between plasma, urine, and renal papillary cyclic AMP content following vasopressin and DDAVP. 22 12

The effect of the diuretics, 1,4-dimorpholino-7-phenylpyrido[3,4-d]pyridazine (DS-511) and its 4'-hydroxy derivative [DS-511(4'-OH)] on the ADH-cyclic AMP system was studied in slices of rat renal medulla. These compounds alone did not affect the basal level of cyclic AMP in the slices. Preincubation with 10(-6) mol DS-511 or 10(-7) to 10(-5) mol DS-511-(4'-OH) in the presence of theophylline, inhibited arginine vasopressin stimulated formation of cyclic AMP, but after washing the slices the formation was restored. Etacrynic acid required higher concentrations such as 10(-5) and 10(4-) mol to cause inhibition. No effect was observed with furosemide and hydrochlorothiazide in concentrations up to 10(-4) mol. DS-511(4'-OH) at concentrations higher than 10(-6) mol inhibited the activity of cyclic AMP-phosphodiesterase in the medullary homogenate. These results suggest the water diuretic action of DS-511 is partly mediated by its inhibition of the ADH-cyclic AMP system.
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PMID:Effect of the diuretic, 1,4-dimorpholino-7-phenylpyrido[3,4-d]-pyridazine (DS-511) and its derivatives on ADH-cyclic AMP system in rat renal medullary slices. 22 1

Tritiated water (3H2O) exchange was shown to be more sensitive to circulatory changes than to arginine vasopressin (ADH)-induced permeability changes. Reducing the circulation (sciatic artery ligation) and increasing the circulation (severing the sciatic nerve) caused the 3H2O exchange in frog legs to decrease from 6.0 +/- 1.3 (5) to 3.5 +/- 0.5 and increase from 6.0 +/- 0.7 (10) to 8.6 +/- 0.6 ml.h-1, respectively. In contrast injection of ADH caused a negligible increase in 3H2O exchange from whole frogs, while at the same time causing a significant increase in osmotic water exchange from 0.22 +/- 0.08 (6) to 0.63 +/- 0.13 (6) g.100 cm-2.h-1.200 mosM-1. Circulatory changes in whole frogs were produced by inducing a diving bradycardia that was less pronounced in a bath aerated with oxygen than with air. The bradycardia caused a reduction in skin circulation, as measured by 3H2O exchange, from 0.210 +/- 0.007 (16) to 0.17 +/- 0.006 (16) ml.h-1.cm-2 in air mixed media and from 0.149 +/- 0.009 (16) to 0.135 +/- 0.011 (16) in oxygen mixed media. Diving bradycardia was also found to affect osmotic water uptake which decreased from 0.61 +/- 0.05 (16) to 0.39 +/- 0.03 (16) g.100 cm-2.h-1.200 mosM-1 in air mixed media and from 0.61 +/- 0.05 (16) to 0.51 +/- 0.04 (16) in oxygen mixed media. The results indicate that circulation affects osmotic water exchange.
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PMID:Circulatory effects on osmotic water exchange in Rana pipiens. 30 2

Plasma and urinary arginine vasopressin (AVP) in normal subjects and in patients with various water metabolism disorders was measured using a sensitive, specific radioimmunoassay. The AVP plasma levels in normal subjects were 3.1 +/- 1.2 pg/ml. The parallel changes in plasma osmolality, plasma AVP concentration, and urinary osmolality were observed after water load. In patients with various kinds of hyponatremia and impaired water excretion, plasma AVP concentrations were within or over normal levels, suggesting that persistent secretion of AVP may play an important role in the pathogenesis of hyponatremia. Variable levels of plasma AVP were observed in patients with essential hypernatremia, which in turn suggested that osmoreceptors may be selectively damaged in some patients, and that ADH-secreting neurons are also involved in others. Our radioimmunoassay facility made it possible for us to measure plasma and urinary DDAVP in the treatment of diabetes insipidus.
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PMID:Application of vasopressin radioimmunoassay to clinical study: role of vasopressin in hypo- and hypernatremia and some other disorders of water metabolism. 66 88

Inhibition of ADH-secretion and transient water diuresis was observed as acute effects of radio-frequency lesions in the septal region of goats. The water diuresis was not compensated for by drinking and therefore rapidly induced pronounced hypernatremia and hypovolemia. The development of hypovolemia was accompanied by a rise in plasma renin activity. Lesions of the same kind, but extending into the preoptic region near the medial portion of the supraoptic nuclei induced the inability to excrete excessive water characteristic of SIADH. Determinations of plasma arginine vasopressin suggested that the lesions causing SIADH did not produce any noticeable increase in basic ADH-secretion. The results suggest that impulses from juxtaventricular receptors regulating ADH-release and water intake to a considerable extent are transmitted via the septal region, and that elimination of this impulse traffic is sufficient to turn water balance to the negative side. However, reflex volumetric inhibition of the ADH-secretion does not seem to be mediated by pathways passing through the septal region.
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PMID:Transient water diuresis and syndrome of inappropriate antidiuretic hormone secretion (SIADH) induced by forebrain lesions of different location. 71 63

During the onset of malignant hypertension (MH) in rats treated with deoxycorticosterone trimethylacetate (DOC), plasma arginine vasopressin (AVP) concentrations increase tenfold as a consequence of hypovolemia and hyperosmolality. In benign hypertensive (BH) rats, plasma AVP is increased threefold in comparison with control animals. Plasma renin is markedly suppressed in both BH and MH animals. In MH rats, biologically active AVP antiserum lowers blood pressure (BP) transiently to normal or subnormal levels; in BH rats, a small BP-lowering effect of the AVP antiserum is seen. (Biologically active angiotensin II antiserum does not lower BP in MH rats.) The relationship between the height of BP and plasma AVP concentration in DOC hypertensive rats indicates, when compared with that relationship in diabetes insipidus rats infused with AVP, a marked enhancement of the vasopressor effect of AVP. These findings and the earlier observation of vasopressin-induced vascular damage by Byrom (F. B. Byrom, The Hypertensive Vascular Crisis. London: Heinemann, 1969) strongly suggest that ADH is involved as a vasopressor hormone in the pathogenesis of malignant DOC hypertension.
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PMID:Vasopressor role of ADH in the pathogenesis of malignant DOC hypertension. 84 73

The treatment of a patient with diabetes insipidus (DI) is described, and the general treatment of the syndrome is reviewed. The patient was a 16-year-old male who had experienced pain, inflammation and tenderness in the left gluteal region owing to an abcess at the site of intramuscular injection of vasopressin tannate in oil (VTO). (He had been diagnosed as having DI at age 8. Since then, he had been maintained on VTO, lypressin and posterior pituitary snuff.) After the abscess healed during hospital treatment, VTO was stopped and the patient's urinary output increased sharply; urine specific gravity and osmolarity decreased correspondingly. Three days after stopping VTO, the investigational drug, 1-deamino-8-D-arginine vasopressin (DDAVP), was begun at 10 microgram every 12 hours. The dose was eventually increased to 20 microgram every 12 hours, and the patient was discharged on this regimen which controlled his urine output, specific gravity and osmolarity. Other treatments reviewed include antidiuretic-hormone-replacement agents (vasopressin, lypressin) and drugs used to potentiate low ADH levels (chlorpropamide, clofibrate and carbamazepine).
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PMID:Treatment of diabetes insipidus with DDAVP. 90 88

A study of plasma arginine vasopressin in 17 patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH) associated with bronchogenic carcinoma, revealed that the arginine vasopressin levels were distinctly elevated in most. In 14 patients with bronchogenic carcinoma, but without overt SIADH, plasma levels of arginine vasopressin were significantly higher than in normal subjects (p less than 0.001). This, together with the finding of a lower than normal plasma osmolality in this group, suggests that inappropriate ADH excess might be much more common in patients with bronchogenic carcinoma than previously thought. The normal positive correlation between plasma osmolality and plasma arginine vasopressin was found to be reversed in SIADH. Seven of nine patients with overt SIADH, studied after fluid deprivation, showed an increase in plasma arginine vasopressin coincident with an increase in plasma osmolality (r = +0.8, p less than 0.01); in one patient, plasma arginine vasopressin returned to the original level following rehydration. The possibility that this might imply a degree of physiologic control to what is generally considered an autonomous secretion is discussed. It is, however, considered more likely that other factors, including changes in plasma volume and glomerular filtration, might explain the increase in plasma levels of arginine vasopressin.
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PMID:Plasma arginine vasopressin in the syndrome of antidiuretic hormone excess associated with bronchogenic carcinoma. 100 69

The effect on water metabolism of 1-deamino-8-D-arginine vasopressin and lysine vasopressin have been studied and compared in 20 vasopressin-sensitive and 2 ADH-resistant diabetes insipidus patients. In every case of ADH-sensitive diabetes insipidus, diuresis decreased and the urinary osmolality increased more markedly and for a longer time with the former than with the latter drug. Both drugs were ineffective in patients with ADH-resistant diabetes insipidus. Administration of 1-deamino-8-D-arginine vasopressin did not cause any side effect. It is concluded that 1-deamino-8-D-arginine vasopressin can successfully be employed in the treatment of ADH-sensitive diabetes insipidus.
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PMID:Treatment of diabetes insipidus with 1-deamino-8-d-arginine vasopressin. 123 63


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