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)

In 35 patients with normal renal function antidiuretic hormone (DDAVP) effected a significant contraction of renal pelvis and calices, while in 10 other cases an enlargement of the roentgenological size of the kidneys was caused by the administration of the diuretic furosemide (Lasix). These results suggest a dependence of urographic findings from the state of diuresis.
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PMID:[Urographic effects of different states of diuresis (author's transl)]. 13 53

Na+-K+-ATPase was inhibited by 1 times 10-4M ethacrynic acid and mercuderamide, and by 1 times 10-3M hydrochlorothiazide and furosemide. A modification of Gilman's (1970) protein displacement assay has been used to measure c-AMP levels in toad bladder epithelial cells. Vasopressin (50 mU/ml) caused c-AMP levels to rise from 4.27 to 9.27 pmol/mg protein. Ethacrynic acid had no effect on cellular c-AMP levels after 10 min exposure to the drug, but at 90 min caused a reduction of both basal and vasopressin stimulated levels. Furosemide caused an apparent rise in c-AMP levels, dilution ratio measurements indicated interference by this drug in the assay procedure, mecuderamide also caused substantial interference with the c-AMP assay. Hydrochlorothiazide had no effect on basal or hormone stimulated levels of c-AMP. It was concluded that the inhibition of sodium transport produced by ethacrynic acid in toad bladder is probably due to inhibition of adenylate cyclase, an effect not shared by other dieuretics.
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PMID:The effect of diuretics on Na+-K+-ATPase and c-AMP levels in toad bladder epithelial cells. 16 90

The effect of furosemide and amiloride on the transport of sodium, potassium, hydrogen and bicarbonate ions was studied in microperfusion experiments on the main excretory duct of the submaxillary gland of the rat. Furosemide did not impair transport of Na+, K+ and H+/HCO-3. Amiloride, however, completely abolished Na+ transport. Blockade of Na+ transport was accompanied by abolition of passive K+ secretion, whereas the active components of K+ and HCO-3 secretion were not affected. In urinary excretion studies, amiloride, which is known to block sodium transport selectively, was used in order to assess whether furosemide has a distinct effect that is independent of sodium transport. Oral administration of amiloride caused a selective excretion of Na+ in a more alkaline urine with an extremely low K+ concentration. The injection of furosemide caused a copious diuresis of an isotonic urine, in which excretion of Na+ and K+ was balanced by the excretion of Cl- ions. Combined administration of amiloride and furosemide produced summation of the individual effects of both diuretics, indicating that the two drugs had different sites and modes of action. In the presence of furosemide the kidney no longer responded to antidiuretic hormone, which suggested that the urine concentrating mechanism in Henle's loop was blocked by furosemide.
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PMID:The separate modes and sites of action of furosemide and amiloride. 23 80

The effects of ouabain, vasopressin, and furosemide on intracellular concentrations of total sodium([Na]) and potassium [K]), on exchangeable sodium ([Na]) and the sodium transport pool ([Nap]) were investigated in isolated short circuited skins of rana esculenta. Furosemide was added to the epithelial bathing solution, vasopressin and ouabain to the corial bathing solution. Results were compared with the amount of net sodium transport measured by short circuit current (scc). Ouabain reduces scc and increases [Na] and [Na]; [K] is decreased. The administration of vasopressin leads to a sharp increase of scc, combined with an enhancement of of [Na] and [Na]; [K] shows no significant change. [Nap] is significantly increased, too, and approximately to the same amount as [Na]. Furosemide causes an increase of scc, whereas a significant change of [Na], [Na] and [K] could not be detected. On the other hand, [Nap] was enhanced significantly. The results support the hypothesis that furosemide like vasopressin is acting by increasing the entry of sodium into the transport compartment of the active cell layer. The result is an increased transfer of sodium across the skin.
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PMID:Effects of furosemide on sodium content and transport pool in frog skin (Rana esculenta): comparison with vasopressin and ouabain. 108 Dec 3

1. To assess whether or not lignocaine influences baseline and frusemide-induced (5 mg kg-1) plasma concentrations of arginine-vasopressin (AVP), 2 groups of rabbits received an infusion of lignocaine (130 micrograms min-1 kg-1) for 6 h. Lignocaine-induced changes in AVP plasma concentrations were substantiated by measurement of diuresis and natriuresis and hepatic plasma flow, by means of an infusion of indocyanine green (ICG) (249 micrograms min-1 kg-1). 2. Baseline plasma AVP levels were 4.9 +/- 0.9 pg ml-1 (+/- s.e.), and following lignocaine, these values were reduced to 0.7 +/- 0.1 pg ml-1 (P less than 0.01). Frusemide increased AVP levels to 134.1 +/- 73.6 pg ml-1 (P less than 0.05) and lignocaine totally prevented this increase, e.g. mean AVP levels of 2.7 pg ml-1. 3. Lignocaine enhanced baseline diuresis secondary to an increase in free water clearance; none of the experimental conditions affected the diuresis and natriuresis induced by frusemide. 4. Frusemide reduced the hepatic plasma flow and this decrease was not reversed by the infusion of lignocaine. 5. It is concluded that in healthy rabbits lignocaine reduces baseline secretion of AVP and its antidiuretic effect; in addition, lignocaine prevents the rise in AVP induced by frusemide.
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PMID:Effect of lignocaine on arginine-vasopressin plasma levels: baseline or induced by frusemide. 139 72

The hypothesis that the greater CT enhancement of the renal medulla relative to cortex after the administration of perfluorooctylbromide (PFOB) was due to the renal medullary osmotic gradient was tested in eight dogs infused with 10 g/kg PFOB. Urine osmolarity and CT attenuation of the cortex and medulla of each kidney under the full effect of antidiuretic hormone were measured before and after 40 mg of furosemide given intravenously, which is known to destroy the renal osmotic gradient. In an attempt to measure the fractional blood volume of the cortex and medulla, which could account for the observed difference on CT, 10 mCi of 99mTc-labeled erythrocytes were given and cortical and papillary tip tissue samples harvested within 1 minute of the animals' death. Cortical blood volume was eight times that of the medulla (21.6 +/- 5.1% vs 2.7 +/- 0.5%, P less than 0.01) and was not significantly affected by furosemide. Furosemide markedly decreased urine osmolarity (1473 +/- 176 mOsm to 454 +/- 45 mOsm, P less than 0.01), had a minor effect on cortical attenuation (decreased from 90.4 +/- 8.2 to 85.1 +/- 8.1 HU, P less than 0.01), and a marked effect on medullary attenuation (decreased from 140.9 +/- 12.4 to 85.9 +/- 8.9 HU, P less than 0.01) which resulted in total loss of corticomedullary contrast (decreased from 20.0 +/- 3.1% to 0.1 +/- 2.2%, P less than 0.01). Thus, the observed greater CT attenuation of the medulla than cortex following the administration of PFOB, a blood pool agent, is due to the osmotic gradient across the medulla which increases the concentration of the agent in the vasa rectae.
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PMID:AUR Memorial Award 1990. The physiologic basis of the radiodense renal medulla after the administration of blood pool contrast agent PFOB. 227 7

Fractional excretion of lithium (FELi+) has been proposed as an index of fluid delivery to the distal nephron. The increase in FELi+ after the "loop diuretic" furosemide indicates that this postulate may not be valid unless furosemide acts in the proximal tubules. We studied the effect of furosemide (40 mg iv as bolus, followed by 20 mg/h infusion for 90 min) in eight healthy male subjects during maximal water diuresis. Special care was taken to exactly replace urinary losses. Furosemide greatly increased fractional excretion of sodium, from 1.3 +/- 0.4 to 27.8 +/- 3.9%, and water, from 14.2 +/- 1.7 to 38.2 +/- 3.7% (P less than 0.01). There was a disproportionately large increase in FELi+ from 30.3 +/- 3.0 to 53.7 +/- 2.9% (P less than 0.01), whereas fractional excretion of some other alleged proximal markers increased to a lesser extent. Lysine vasopressin, infused at the end of the experiment (n = 7), caused only a small increase in urine osmolality from 225 +/- 17 to 241 +/- 17 mosmol/kg (P less than 0.01), indicating that medullary hyperosmolality had been largely abolished. The most likely explanation of these results is that furosemide has a moderate action in the proximal tubules, and at the same time inhibits preexistent lithium absorption in Henle's loop. In addition, the large difference between FELi+ and maximal urine flow remaining after furosemide suggests that, despite the decreased medullary osmotic gradient, water backdiffusion is unaltered by furosemide or that lithium concentration in the proximal tubule is changed by furosemide.
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PMID:Does lithium clearance reflect distal delivery in humans? Analysis with furosemide infusion. 233 Sep 75

The present in vitro microperfusion study examined whether furosemide has an effect on hydraulic conductivity (Lp X 10(-6) cm/sec.atm) and 14C-urea permeability (Pu X 10(-5) cm/sec) in inner medullary collecting ducts (IMCD) and cortical collecting tubules (CCT) isolated from rat and rabbit kidneys. Furosemide added to the bath fluid decreased arginine-vasopressin (AVP)-stimulated Lp of rat IMCD in a dose-dependent manner, with the threshold effect at 10(-6) M. Furosemide (10(-4) M) reduced Lp from 20.5 +/- 2.3 to 12.1 +/- 1.2 (P less than 0.01) reversibility, but had no effect when added to the perfusate. In addition, furosemide reduced dibutyryl cyclic AMP-stimulated Lp from 20.3 +/- 1.1 to 11.2 +/- 1.6 (P less than 0.01). This effect of furosemide was also observed with indomethacin, a PGE2 synthesis inhibitor. The addition of indomethacin (10(-4) M) to AVP (50 microU/ml) increased Lp from 24.7 +/- 2.3 to 29.7 +/- 2.8 (P less than 0.001), which was reduced to 20.3 +/- 2.6 (P less than 0.001) when furosemide was added to indomethacin in the bath. The inhibitory effect of furosemide on AVP-stimulated Lp was also observed in rabbit IMCD (Lp decreased from 12.8 +/- 0.8 to 5.15 +/- 1.46, P less than 0.02), but it was not observed in the CCT isolated from rabbit kidneys (7.96 +/- 1.87 with AVP vs. 7.94 +/- 1.41 with AVP + furosemide). Furthermore, in rat IMCD the stimulatory effect of AVP on Pu from 7.7 +/- 0.4 to 26.8 +/- 1.3 was reduced by furosemide to 19.7 +/- 1.2 (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of furosemide on water and urea transport in cortical and inner medullary collecting duct. 234 23

This study examined the possible existence and nature of Ca2+ transport in frog skin using 45Ca fluxes and short-circuiting technique. Following the addition to full-thickness frog skin (FTFS) of 8-[p-chlorophenylthio]cAMP (8-CPT-cAMP), forskolin, or 1-methyl-3-isobutylxanthine, the secretory Ca2+ flux increased severalfold, inducing net Ca2+ secretion. The absorptive flux was unchanged. Isoproterenol (10(-6)M) reproduced the effects of cAMP on Ca2+ secretion (-3.76 +/- 0.80 nmol X cm-2 X h-1 vs. +0.04 +/- 0.05 in control) while vasopressin and parathyroid hormone did not alter Ca2+ fluxes. Because FTFS contains subepidermal glands capable of Cl- secretion in response to beta-adrenergic stimulation, split-thickness frog skin (STFS) consisting of the gland-free Na-absorbing surface epithelium was used to localize the anatomic site of Ca2+ secretion. In STFS, addition of 8-CPT-cAMP or isoproterenol failed to induce Ca2+ secretion, suggesting that this transport in FTFS is localized in skin glands. Additional studies explored the relationship between Ca2+ and Cl- transport in FTFS. Furosemide prevented the stimulation of both Ca2+ and Cl- secretion. Removal of Cl- from the bathing medium abolished Ca2+ secretion. Thus, FTFS exhibits a beta-adrenergic, cAMP-stimulated net Ca2+ secretion that is Cl- dependent. As this effect is not observed in STFS, the pathway of Ca2+ secretion in frog skin is probably localized in the subepidermal glandular epithelium in association with Cl- secretion. Frog skin glands may represent a useful model for the study of Ca2+ transport in Cl--transporting epithelia.
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PMID:cAMP- and beta-adrenergic-stimulated chloride-dependent Ca2+ secretion in frog skin. 241 6

Plasma levels of atrial natriuretic peptide (ANP), aldosterone (PA), vasopressin (AVP), and the plasma renin activity (PRA) were examined in 15 vascularly decompensated patients suffering from liver cirrhosis, before and after administration of albumin and after a subsequent administration of furosemide. The initial ANP level was lower in 9 patients (group "A") and higher in 6 patients (group "B") than in healthy controls (Group "A": 19.5 +/- 3.0 fmol/ml; group "B": 36.7 +/- 3.9 fmol/ml; control: 25.8 +/- 2.4 fmol/ml). The initial PRA (4.4 +/- 1.0 ng AngI/ml/h) and AVP (8.5 +/- 1.5 pg/ml) activity in group "A" increased significantly compared to group "B" (PRA: 0.44 +/- 0.09; AVP: 4.1 +/- 0.5), indicating an intravascular volume depletion in group "A". Albumin infusion raised the urine and sodium excretion and the plasma concentration of ANP in group "A" but lowered in plasma levels of renin and vasopressin. The same parameters were not changed by albumin in group "B". Furosemide equally raised the urine flow rate and sodium excretion in both groups. Plasma ANP level depends on the intravascular volume, and the secondary change in its plasma concentration plays a considerable role in the retention of fluid and electrolytes in patients with cirrhosis. The increased intravascular volume in these patients depletes the fluid and electrolyte retention via the increase in ANP level.
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PMID:Alterations of vasoconstrictor and sodium-regulating hormone systems in vascularly decompensated liver cirrhosis. 297 Jun 21


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