Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

dl-Propranolol (0.8-1.6 mg/kg - h for 1 h) produced a transient two- to three-fold increase in sodium excretion in nondiuretic rats infused with Pitressin and aldosterone and in water diuretic rats. Sodium excretion increased more in rats depleted of renin by chronic Doca and salt administration than in rats maintained on a low salt diet. An angiotensin inhibitor (1,sarcosine-8,valine angiotensin II) decreased sodium excretion. Therefore the natriuresis was not mediated by antidiuretic hormone, aldosterone, or renin-angiotensin. d-Propranolol did not produce a natriuresis. Prior treatment with phenoxybenzamine did not prevent the natriuretic response but chlorisondamine pretreatment did. The natriuresis is produced by beta blockade and requires post ganglionic nerve function but is independent of alpha receptors. dl-Propranolol decreased heart rate and cardiac output but systemic pressure did not fall and renal blood flow increased. This suggests a dopamine-mediated renal vasodilation and natriuresis. Haloperidol and pimozide, both dopamine blocking agents with minimal beta blocking effects, prevented the natriuretic response. We conclude that propranolol may increase sodium excretion directly by blocking beta receptors in the distal nephron and indirectly by dopamine-mediated renal vasodilation.
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PMID:Propranolol induces acute natriuresis by beta blockade and dopaminergic stimulation. 1 Oct 39

Using Brattleboro rats with and without hereditary diabetes insipidus (DI, non-DI), blood pressure, water intake and the excretion of water, sodium, potassium and osmotically active substances were measured in intact individuals and in animals subjected to unilateral nephrectomy at the age of 23 or 80 days. The development of blood pressure (BP) changes, determined in unilaterally nephrectomized animals at the age of 4--6 months, depended on the age at which the kidney was removed. After nephrectomy at the age of 25 days, hypertension developed only in DI females given 0.6% NaCl solution to drink. The BP of those which drank water was unaffected. Unilateral nephrectomy at the age of 80 days produced a slight BP increase in females irrespective of whether they drank water or 0.6% NaCl, but in males only if they drank 0.6% NaCl solution. No hypertension was observed in intact animals. No relationship was found between water intake and the blood pressure level. The BP increase in water-drinking females uninephrectomized at 80 days was accompanied by a raised urine flow and raised excretion of osmotically active substances. Sodium losses in DI animals were greater than in non-DI animals and the urinary sodium concentration, in maximum dehydration, attained minimum values in DI and maximum values in non-DI animals. Unilateral nephrectomy at 25 days increased sodium losses in all the animals except non-DI females, but when performed at 80 days, only in DI males. No relationship between these results and BP changes was found. The possible relationship of the extrarenal consequences of absence of vasopressin to the development of experimental hypertension are discussed.
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PMID:Blood pressure and water and electrolyte intake and excretion in rats (Brattleboro strain) after unilateral nephrectomy. 14 74

1 The effect of intravenous infusion of lithium, 2.56 mumol/min on the antidiuretic responses to antidiuretic hormone (ADH), adenosine triphosphate (ATP), 3'-5' adenosine cylic monophosphate (cyclic AMP) and theophyline was studied in water-loaded, alcohol-anaesthetized rats. 2 Lithium reversibly inhibits the antidiuretic response to all concentrations of ADH, depressing the maximum response but not changing the amount required for half maximal response. 3 The rate of increase of serum lithium relates more clearly to the inhibitory effect than does the serum concentration. 4 Sodium concentrations in the renal papilla seem to fall when serum lithium levels are rising. 5 Lithium inhibits the antidiuretic response to ATP and cyclic AMP but does not inhibit the response to theophyline.
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PMID:The effects of lithium ions on the antidiuretic action of vasopressin in the rat. 17 68

1. Sodium transport across isolated frog skin, as measured by the short-circuit current, was decreased by acetylsalicylic acid, mefenamic acid, paracetamol and phenylbutazone. Indomethacin (6 X 10(-6) M) had a biphasic effect on the short-circuit current: a transient increase followed by a sustained decrease. 2. The release of prostaglandin-like material from the skin was reduced by acetylsalicylic acid and indomethacin. Paracetamol caused a significant reduction in the short-circuit current response of the skin to low doses of arachidonic acid, but the response to the highest dose tested was not significantly altered. 3. Indomethacin (6 X 10(-6) M) increased the sensitivity of the skin to applied prostaglandin E1. The other prostaglandin synthetase inhibitors did not have this effect. Indomethacin (6 X 10(-6) M) also enhanced the effect of antidiuretic hormone on the short-circuit current. 4. Indomethacin (30 X 10(-6) M) increased the short-circuit current and diminished the response to applied prostaglandin E1. 5. In sulphate Ringer, theophylline increased the short-circuit current and diminished the response to prostaglandin E1. 6. Prostaglandin E1 increased the levels of cyclic AMP in frog skin and these increases preceded the increases in short-circuit current. There was a seasonal variation in the level of cyclic AMP in the skin: the levels in winter exceeded those in summer. There was also a seasonal variation in the cyclic AMP response to prostaglandin E1: the winter response was greater than that in summer. 7. Indomethacin (6 X 10(-6) M) had a biphasic effect on cyclic AMP levels in the skin, an initial increase followed by a decrease. Indomethacin also potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 8. Theophylline increased cyclic AMP levels in the skin and potentiated prostaglandin E1 stimulated cyclic AMP accumulation. 9. Pre-treatment of the skin with theophylline reversed the effects of cyclic AMP on the short-circuit current and open-circuit potential. 10. It is concluded that endogenous prostaglandins help to maintain sodium transport across isolated frog skin and that the effects of E-type prostaglandins on the short-circuit current are mediated by increased cyclic AMP levels. The transient increase in short-circuit current and the increased skin sensitivity caused by indomethacin (6 X 10(-6) M) are attributed to inhibition of phosphodiesterase activity. The failure of theophylline to potentiate the short-circuit current response of the skin to prostaglandin E1 is attributed to alteration of cyclic AMP action on the skin by theophylline.
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PMID:Endogenous prostaglandins, adenosine 3':5'-monophosphate and sodium transport across isolated frog skin. 18 63

The calcium ion concentration measured in rat kidney mitochondria, isolated from vasopressin treated tissue, has a dose response characteristic in which the calcium concentration reached a minimum at low doses of vasopressin (2 mU/ml), at higher doses of hormone the mitochondrial calcium ion concentration increases reaching a value close to that of the controls with vasopressin (100 mU/ml). This efflux and subsequent uptake of mitochondrial calcium has been shown to be a direct effect of the varying cyclic AMP concentrations. Sodium and water permeability effects of vasopressin have been shown in toad bladder to have different dose response characteristics. Maximum sodium transport occurs at a lower dose of vasopressin (2 mU/ml) and is believed to be associated with direct permeability effects of the hormone. Maximum water transport occurs at a higher dose of vasopressin (100 mU/ml) over a concentration range associated with hormone-stimulated adenylate cyclase activity. The water transport response to low doses of vasopressin may be potentiated by aldosterone treatment, an effect that can be related to the inhibition of tissue phosphodiesterase activity and subsequent increased cyclic AMP concentrations. In steroid depleted conditions the cyclic AMP medicate efflux of mitochondrial calcium ions, that occurs at low doses of vasopressin, may prevent the release of membrane bound calcium ions and thus inhibit the water permeability effect of the hormone. Higher levels of cyclic AMP reverse this inhibitory effect and give rise to an increased water flow. It is concluded that cyclic AMP and intracellular concentrations of calcium ion act as inter-related mediators of antidiuretic hormone action.
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PMID:Role of mitochondrial Ca2+ in antidiuretic hormone action. 18 79

Adenylate cyclase (AC) and phosphodiesterase (PDE) activities were studied in the cortex, medulla and papilla of the rat kidney. Sodium loading in vivo for 14 days resulted in a decrease of AC activity in the cortex, a small increase in the medulla and a substantial increase of AC activity in the papilla. Sodium loading caused reciprocal effects on PDE activity: an increase in kidney cortex and a decrease in kidney papilla. Loading of glucose in vivo or chronic administration of antidiuretic hormone in vivo did not cause the changes in AC or PDE observed after sodium loading. The possible significance of these findings is discussed.
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PMID:Effect of salt loading in the rat on adenylate cyclase and phosphodiesterase activity in kidney cortex, medulla and papilla. 19 46

The effects of intravenous infusion of ornithine-vasopressin (OVP) and desamino-D-arginine-vasopressin (dDAVP) were studied in normal and hydrated Merino sheep. In normal sheep, OVP resulted in a diuresis, increased urinary sodium and potassium excretion, and a fall in the plasma potassium concentration. Renal plasma flow remained constant but glomerular filtration rate and filtration fraction rose markedly. dDAVP in normal sheep was antidiuretic, but its only significant effect was a small decrease in plasma osmolality. In the hydrated sheep OVP was antidiuretic and resulted in increased urinary excretion of sodium and potassium, and a fall in the plasma potassium level. Renal plasma flow fell, but glomerular filtration and filtration fraction tended to rise. dDAVP in the hydrated sheep was also antidiuretic but urinary sodium and potassium excretion was reduced. Renal plasma flow and glomerular filtration fell, with a small decrease in filtration fraction. These results suggest that the diuretic effect in normal sheep and the electrolyte-excreting effects in both normal and hydrated sheep of OVP are related to the increase in glomerular filtration, which in turn is dependent on the vasopressor activity of the hormone. The increase in glomerular filtration caused by OVP is due to an increase in the filtration fraction of an unchanged renal plasma flow, which could be brought about by an increase in renal efferent arteriolar tone. The effects of hydration of the sheep were the conventional increased urine flow, decreased urine osmolality and decreased solute-free water reabsorption. Sodium and potassium excretion rose slightly and plasma osmolality fell. Renal plasma flow and glomerular filtration both increased with little change in filtration fraction. These effects could be brought about by suppression of endogenous vasopressin and a decrease in both afferent and efferent renal arteriolar tone.
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PMID:The effects of two analogues of arginine-vasopressin (ornithine-vasopressin and desamino-D-arginine-vasopressin) on kidney function in sheep. 24 35

The authors determined cardiovascular, renal, and hormonal responses to increased airway pressure during continuous positive-pressure ventilation (CPPV) and continuous positive airway pressure (CPAP). Nine healthy, hydrated laboratory swine had appropriate catheters placed to allow for measurement of intrapleural, aortic, inferior vena caval, and left ventricular end-diastolic pressures; cardiac output; and urinary flow. Samples of arterial blood were analyzed for oxygen and carbon dioxide tensions, pH, plasma vasopressin, osmolality, and creatinine and sodium concentrations. Urine was analyzed for osmolality and creatinine and sodium concentrations, and volume was recorded. Intrapleural pressure was subtracted from left ventricular end-diastolic pressure to calculate transmural pressure, a reflection of left ventricular filling pressure. Glomerular filtration rate and urinary free-water and osmolal clearances were also calculated. Expiratory left ventricular filling pressure was decreased equally by CPAP and CPPV. However, inspiratory left ventricular filling pressure and cardiac output were decreased by CPPV only. Urinary flow and glomerular filtration rate were decreased equally by CPAP and CPPV. Sodium excretion was decreased and plasma vasopressin increased by CPPV, but not by CPAP. Urinary free water and osmolal clearances were not changed by either ventilatory pattern. Although many of the renal-function variables were affected similarly by CPPV and CPAP, these alterations were not influenced solely by cardiac output or vasopressin, because only CPPV depressed cardiac output and increased vasopressin levels.
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PMID:Renal function and cardiovascular responses during positive airway pressure. 37 28

Acetazolamide concentration values derived from a nonlinear model system were related to two pharmacological responses in the rabbit. Kidney response was measured by monitoring urine flow and sodium elimination. Ocular response was followed using an applanation tonometer. Maximum urine flow and sodium elimination occurring immediately after injection correlated with log dose. Urine flow dropped below control values along with a rise in osmolality, suggesting the involvement of antidiuretic hormone. Sodium elimination was correlated with plasma levels. Urine pH is thought to be involved in reducing accessibility of drug to carbonic anhydrase in the kidney. Maximum ocular response also was correlated with log dose. Ocular response was related to a protein fraction, which is believed to be mainly carbonic anhydrase. However, the duration of ocular response was related to the red blood cell protein fraction. Thus, drug activity could conceivably be regulated by monitoring a tissue that is not the site of action and can be sampled readily.
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PMID:Relationship of pharmacokinetics to pharmacological response for acetazolamide. 42 26

Sodium and water retention is constant in decompensated cirrhosis with ascites and edema. Sodium retention is due to several factors. Renal hemodynamic disturbances appear first: decrease in glomerular filtration and renal plasmatic perfusion, redistribution of renal perfusion to the juxtamedullar area where the longer nephrons reabsorb more sodium. Metabolic disorders of estrogens, natriuretic hormonal factor, prostaglandins and the kallikrein-kinin system contribute to greater sodium retention. Water retention is secondary to greater sodium reabsorption and to hyperactivity of the antidiuretic hormone. Sodium and water retention, associated with portal hypertension, with reduced oncotic pressure and with dynamic lymphatic insufficiency, is responsible for the production of ascites. The latter results in a decrease in the effective plasmatic volume, with non-suppression of the renin-angiotensin system, increased aldosterone production and additional sodium retention.
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PMID:[The physiopathology of ascites]. 46 62


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