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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report two cases and consider the various physiopathological mechanisms of inappropriate hypersecretion of antidiuretic hormone. An exploration including clearance of free water and, in some cases, estimation of ADH before and after a water load, then before and after administration of ethyl alcohol, permits one to determine the mechanism. It seems advisable to reserve the term Schwartz-Bartter syndrome to paraneoplasic syndromes linked to ectopic and autonomous secretion of ADH.
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PMID:[Inappropriate secretion of antidiuretic hormone: true and false Schwartz-Bartter syndrome. Apropos of 2 cases]. 19 21

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 role of pituitary vasopressin (antidiuretic hormone--ADH) in the formation and dynamics of aqueous humour was studied in rabbits employing different techniques. Using isolated ciliary body preparations the changes in transepithelial short-circuit current were measured, and natural vasopressin and Lys8-vasopressin were found to increase the transepithelial short-circuit current at concentrations less than 10 muU/ml (i.e. within the physiological range), indicating increased sodium transport across the ciliary epithelium. In another series of experiments with intact rabbits given an ethanol load to suppress endogenous ADH, administration of exogenous vasopressin raised the intraocular pressure, and a similar effect was observed when endogenous ADH production was stimulated with nicotine. Direct measurements of outflow showed that vasopressin was without effect when given intravenously and that the only effect when given intracamerally was to increase the facility which would tend to lower rather than raise the intraocular pressure. Finally, the intra-arterial and intravenous effects of vasopressin on circulation in the iris and on the intraocular and systemic arterial pressures were studied. Local effects on the vascular bed in the eye and changes in systemic blood pressure were observed only at rates of administration well in excess of the physiological range for endogenous vasopressin production. It is concluded that, at physiological levels, antidiuretic hormone can stimulate active sodium transport into the eye thereby tending to raise the intraocular pressure, and it is suggested that this may act as a homeostatic regulating mechanism limiting changes in the rate of formation of aqueous humour and in intraocular pressure which might otherwise result from diurnal variations in the state of body hydration. This also offers some explanation for the ocular hypotensive action of ethanol.
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PMID:Role of pituitary vasopressin in the formation and dynamics of aqueous humour. 28 4

Angiotensin II is dipsogenic, and vasopressin (ADH) regulates renal water excretion. Together, these hormones govern overall mammalian water balance. The Brattleboro rat with inherited diabetes insipidus (DI) lacks ADH and is therefore a convenient model with which to elucidate mechanisms regulating water metabolism. In the present studies, angiotensin II has also been removed from DI rats by the administration of an inhibitor (captopril, SQ 14225; D-2-methyl-3-mercaptopropanoyl-L-proline) of the enzyme which converts angiotensin I, the relatively inert component of the renin-angiotensin system, to angiotensin II, the biologically active substance. SQ 14225 reduced the drinking rates, and after 6 days lowered peripheral plasma aldosterone concentrations were associated with hyperkalaemia. We conclude that the polydipsia of diabetes insipidus partly results from elevated plasma renin activities and angiotensin II concentrations seen in this syndrome. Further, the apparent hypoaldosteronism of DI Brattleboro rats reflects differences in both tissue usage of the steroid and adrenocortical sensitivities associated with polyuria, hyperosmolarity and possibly potassium wasting.
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PMID:Captopril (SQ 14225) depresses drinking and aldosterone in rats lacking vasopressin. 38 37

The uptake of C14-urea into everted and noneverted bladder sacs was compared, over short time periods (up to 2 min), with the transepithelial urea fluxes. This method allowed the study of the time course of urea uptake and distribution, while previously this problem was only studied in steady-state conditions. When mucosal uptake was studied no accumulation of C14-urea inside the tissue was observed, indicating that the mucosal border could be the limiting step. Comparative studies of urea and inulin uptake from the serosal side showed that urea equilibrated with the water epithelial cells in less than 30 sec. This accumulation suggested again that the mucosal border is an effective barrier for urea translocation. The kinetics of the increase in urea permeability induced by antidiuretic hormone was also studied and it was similar (T1/2:4.3 min) to the kinetics of the increase in water permeability induced by the hormone (T1/2:5.6 min). A strong parallelism was also observed between the time course of the increases in water and urea permeabilities induced by medium hypertonicity (T1/2 25 and 26 min, respectively). The values obtained for the permeability coefficient ktrans), either at rest or under ADH were similar to those previously reported employing steady-state techniques (28+/-8 and 432+/-25 cm-sec-1-10(-7), respectively).
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PMID:Urea uptake and translocation in toad urinary bladder: the effect of antidiuretic hormone. 40 46

1. The effects of hypertonic saline infusion into the third ventricle were investigated in ten monkeys which were pre-operated, trained, and used in the conscious state under controlled conditions. 2. In non-hydrated monkeys, intraventricular infusion of NaCl 1.0 M, 0.01 ml./min for 30 min did not affect urine volume or Na output but produced a small increase in urine osmolality. Comparable infusion of NaCl 0.15 M had no effect on any parameter. 3. In monkeys undergoing water diuresis (with i.v. infusion of 5% dextrose), intraventricular hypertonic saline produced large reciprocal changes in urine volume and osmolality while urine Na showed no significant change. The effects on urine volume and osmolality were greater than those of lysine-vasopressin 30 m-u./kg i.v. 4. The absence of natriuresis after intraventricular hypertonic saline infusion in the monkey was in notable contrast to the results reported in lower species. However, the data suggested that the infusion probably released ADH as in other species.
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PMID:Search for a natriuretic mechanism sensitive to sodium in the brain of the monkey. 41 58

Experiments were carried out in different segments of the intestine of unanaesthetised rats to assess the effect of vasopressin on intestinal absorptive processes. The following data were observed. (1) Within a physiological range of doses (Aziz, 1969), ADH diminished the net sodium absorption mainly by reducing the unidirectional sodium influx, whereas the behaviour of the efflux was not uniform. (2) The unidirectional volume fluxes showed the same behaviour as did the sodium fluxes. (3) ADH produced an oral-aboral gradient (jejunum greater than ileum greater than colon). (4) ADH did not significantly change the transfer of actively transported sugars; it did influence, however, passively transported substances. (5) During the intravenous application of ADH, a substance was secreted into the perfusion solution which diminished the absorption of volume and electrolytes. (6) Cyclic AMP acted on intestinal absorption in the same way as did ADH. In view of these results two mutually independent transport pathways for sodium and water are supposed, one of which is influenced by ADH or cAMP. Based on a two membrane model, an ADH mechanism is discussed: the permeability of the luminal membrane system is enhanced in the presence of vasopressin.
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PMID:Intestinal absorption under the influence of vasopressin: studies in unanaesthetised rats. 42 21

Despite the apparent absence of vasopressin (ADH), Brattleboro homozygotes [diabetes insipidus (DI) rats] can concentrate their urine when deprived of drinking water. Since other investigators have shown that reducing glomerular filtration rate (GFR) improves the concentrating ability of water-loaded dogs, the present studies were undertaken to quantify the magnitude and time course of changes in GFR during dehydration. Clearance experiments were performed in 10 conscious DI rats before and following 3, 6, 9, 12, 15, and 24 h of dehydration. Urine osmolality increased from 155.0 +/- 12.6 (SE) to 696.7 +/- 8.4 mosmol/kg H2O after 24 h. GFR averaged 984.3 +/- 79.6 microliters . min-1 . 100 g body wt-1 in the control phase, fell to about 80% of this value over the first 12 h of dehydration, and then declined to 27% at 24 h. The rats lost 20% of their body weight over the 24 h. The osmolality of the papillary tip averaged 896 +/- 44 mosmol/kg H2O at 24 h compared to a control value of 493 +/- 28. The lack of osmotic equilibration between urine and papillary interstitium suggests that dehydration did not appreciably increase the water permeability of the distal nephron. These experiments clearly show a progressive decline in GFR as urine becomes concentrated during dehydration in the absence of ADH; these events may or may not be causally related.
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PMID:Urinary concentrating ability during dehydration in the absence of vasopressin. 46 96

Several psychotropic drugs have been associated with the syndrome of inappropriate secretion of antidiuretic hormone (SIADH). We report here a patient who on two occasions developed clinically significant hyponatremia while receiving the antipsychotic drug, haloperidol. The criteria for the syndrome of inappropriate secretion of ADH were fulfilled and other causes of SIADH were excluded. We documented inability in this patient to excrete a water load while on haloperidol and normal ability in its absence. This case therefore illustrates SIADH due to haloperidol.
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PMID:Haloperidol-induced syndrome of inappropriate secretion of antidiuretic hormone. 48 91

In order to investigate the vasopressor role of ADH in the regulation of blood pressure, passive immunization experiments with an antibody to AVP were carried out in experimentally hypertensive rats. In hypertensive rats treated with deoxycorticosterone acetate (DOCA), spontaneously hypertensive rats (SHR) and spontaneously hypertensive stroke-prone rats (SHR-sp), the intravenous injection of a specific vasopressin antibody resulted in a transient fall of blood pressure of 11 approximately 25mmHg, while in rats with two-kidney Goldblatt hypertension and normal rats, the blood pressure was not affected. This strongly suggests that ADH contributed to systemic vaso-constriction in DOCA hypertension and spontaneous hypertension in rats.
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PMID:[The vasopressor role of ADH in the maintenance of blood pressure in experimentally hypertensive rats (author's transl)]. 49 16


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